Without doubt ouabain (g-strophanthin) could be the solution of the problem cardiac infarction to a large extent and especially the therapy with orally administered ouabain and the knowledge about this drug has to be brought forward because of medical, ethical and economic aspects.

Appendix: More unknown pathogenetic aspects of acute myocardial infarction

Because the effect of ouabain is nowadays explainable in both theoretical settings, compatible with the following “new cardiac infarction hypothesis“ as well as with the accepted theory of cardiac infarction, the following controversial standpoints are in fact very interesting, but in comparison to the concrete clinical success of ouabain only a matter of secondary interest, especially if they should provoke disaccord. Dr.med. Berthold Kern, the explorer of the oral ouabain therapy, and the International Society of Infarct Prevention (in the 1960ies up to the 1980ies, see above - the chapter “The solution of the problem is not wanted“) always closely associated the topic “ouabain“ with the “new cardiac infarction hypothesis“ and presented the latter often in a sometimes too unilateral manner, and so the resistance of the official medicine regarding new aspects in the pathogenesis of cardiac infarction was perhaps carried over to the topic of ouabain. Perhaps the “truth“ is a complementary one. In this topic I am not as competent as in the topic of ouabain, and the references are far from beeing complete. (I wish I had the time to read some weeks or months about this fascinating issue.) It is only an attempt to create a new viewpoint in a domain where in the last years many new insights could be won. I hope it is helpful. If you have criticism, please dont “transfuse“ it to the topic of the ouabain medication but rather please inform me ...

A point that has got too little attention is the existance of a coronary artery net inside the heart muscle which is present in every man and woman from birth and is not visible in common angiography. The coronary arteries outside the myocardium, however, are visably constructed like end arteries, with only few collaterals. The intramyocardial coronary artery net consists of countless collaterals and anastomoses. Prof. Baroldi (Washington / Milan) used a special synthetic liquid to perfuse the hearts of human corpses since 1967. After solidification of the liquid he removed all tissue by acid. In that way he made 5000 threedimensional models which revealed the true nature of coronary anatomy (57, 61). Prof. Doerr, the president of the German Society of Pathology at that time, repeated and confirmed the research of Prof. Baroldi in 1974 (65).

The intramyocardial coronary artery net is able to adjust to a stenosis in an extramyocardial coronary artery. In experiments with dogs (180-181, see also 182-183) an immediate and complete ligature of a big coronary branch led to a myocardial infarction in only 50 %. If the coronary ligature was gradually completed over a period of four days, no myocardial infarction was noticed any more, not even an impairment of cardiac output or the ECG. Because the development of coronary arteriosclerosis take place over a much more prolonged period, the significance of a coronary stenosis seen in angiography is put into question by these findings. Autopsy findings from patients with mortal myocardial infarction revealed that the collateral coronary net was always adequately adepted to compensate the stenoses and occlusions of the outer coronary arteries (60-61). The constitution of the intramural coronary net was the same as in patients with comparable outer stenoses and occlusions who had other causes of death (184). A maximal coronary stenosis of > or = 80 % is present in 70 % in coronary ischemic patients and in 38 % in control persons without any clinical sign of ischemia (185). The existance of this artery net should not entice us to overidealise it concerning its function, having in mind for example the possibility of paradox reaction to ischemia (see above, 39-40). There are many studies concerning the endothelial dysfunction, for example due to a reduced nitric oxid (NO). Citation of Schachinger and Zeiher 2000 (186), abstract: “Endothelium-dependent vasodilation is impaired ... mainly due to increased oxidative stress produced by superoxide anions, which rapidly inactivate nitric oxide. Experimentally, an imbalance between nitric oxide and superoxide anions towards reduced nitric oxide bioavailability enhances migration of monocytes into the vessel wall and proliferation of smooth muscle cells.

Citation from Baroldi & Giuliano 1986 (187), abstract: “The high frequency of severe and multivessel atherosclerotic stenosis in non cardiac patients and healthy subjects dying accidentally questions the direct cause-effect relationship between stenosis and ischemic heart disease; supports the view the dramatically enlarged collaterals always found in this condition may have an adequate compensatory role; and suggests the ineffectiveness of occlusion at the site of severe stenosis already bypassed by collaterals. The degree and number of severe stenoses in ischemic heart disease do not predict onset, course, complications, infarct size or death.“ This could perhaps also explain the contradictory findings of Mikkelsson et al. 2004 (188), who reported that in 61 % of fatal myocardial infarctions - having in mind that myocardial necrosis is mostly found in the left ventricle - thrombi were identified in the right coronary artery, although in only 17 % of these cases there was a definite right ventricular infarction. The study discusses a role of right coronary occlusion as a supposed cause of brady-asystolic cardiac arrest, but not the question why these thrombi do not provoke right ventricular necrosis in the other 83 %.

The knowledge about the intramyocardial artery net explains the findings of Ambrose et al. 1988 (189), that myocardial infarction frequently develops from previously nonsevere lesions (remember the experiments with dogs above (180-181, see also 182-183). Citation of Ambrose et al. 1988 (189), abstract: “In this retrospective analysis, progression of coronary artery disease between two cardiac catheterization procedures is described in 38 patients: 23 patients (Group I) who had a myocardial infarction between the two studies and 15 patients (Group II) who presented with one or more new total occlusions at the second study without sustaining an intervening infarction. In Group I the median percent stenosis on the initial angiogram of the artery related to the infarct at restudy was significantly less than the median percent stenosis of lesions that subsequently were the site of a new total occlusion in Group II (48 versus 73.5%, p less than 0.05). In the infarct-related artery in Group I, only 5 (22%) of 23 lesions were initially greater than 70%, whereas in Group II, 11 (61%) of 18 lesions that progressed to total occlusion were initially greater than 70% (p less than 0.01). In Group I, patients who developed a Q wave infarction had less severe narrowing at initial angiography in the subsequent infarct-related artery (34%) than did patients who developed a non-Q wave infarction (80%) (p less than 0.05).“ This indicates that severe, over 70 % stenoses are generally well compensated by collaterals.

The above finding is confirmed by the study of Little et al. 1988 (190), which deals with 42 consecutive patients who had undergone coronary angiography both before and up to a month after suffering an acute myocardial infarction. Citation abstract: “Twenty-nine patients had a newly occluded coronary artery. Twenty-five of these 29 patients had at least one artery with a greater than 50% stenosis on the initial angiogram. However, in 19 of 29 (66%) patients, the artery that subsequently occluded had less than a 50% stenosis on the first angiogram, and in 28 of 29 (97%), the stenosis was less than 70%. ... In only 10 of the 29 (34%) did the infarction occur due to occlusion of the artery that previously contained the most severe stenosis. Furthermore, no correlation existed between the severity of the initial coronary stenosis and the time from the first catheterization until the infarction.“

Also Brown et al. 1986 (191) report about the same phenomenon in 32 patients with myocardial infarction: In 10 cases, this original lesion was less than a 50% stenosis, and in 21 cases less than 60%.

The relatively low incidence of coronary thrombi was just mentioned above (54-66). Citation from Murakami et al. 1998 (54), abstract: “Intracoronary thrombus contributes little to the pathogenesis of average AMI.“ The incidence of thrombi is especially lower in smaller infarcts, for example 8 % in Roberts & Buja 1972 (59) and 27 % in Silver et al. 1980 (56), than in bigger, transmural infarcts (56, 58-59). In addition the thrombi are time-dependent. The longer the period between myocardial infarction and death of the patient, the bigger the frequency of coronary thrombosis (57, 60-66). This could be a indication that the thrombus could be a secondary event. The Swedish cardiologist Erhardt (et al. 1973 and 1976) used an irresistible method: He injected a portion of radioactive labeled fibrinogen into patients after a myocardial infarction. Fibrinogen builds up the thrombus and after this formation there is no exchange of fibrinogen any more. When a patient had died and a thrombus was found, in most cases the radioactivity was present in the whole thrombus, even in the middle section (192-193). This implies that the thrombus was not the cause but the consequence of the myocardial infarction. Prof. Doerr, the president of the German Society of Pathology in the 1970ies, shared the same opinion.

These findings perhaps could be explained by a continuation of the hypothesis of “myocardial infarction by loss of erythrocyte flexibility“ described above (page 6): At first tissue acidification occurs, because of ischemia or myocardial metabolic causes generated by an overstimulated sympathicus (see the next chapter below) or both, which could start the vicious circle of inhibition of Na-K-ATPase and enhanced erythrocyte rigidity which aggravates ischemia, perhaps until a total stop of microcirculation or even developing of a necrosis, without primary occlusion of a coronary branch. This microcirculatory stasis could lead to a tailback of blood in the proximal coronary system which could facilitate the formation of a coronary thrombus at a location of a coronary artery which is narrowed formerly, especially when the infarcted heart cannot build up the normal pressure of blood flowing from the aorta into the coronary system.

A “live report“ of an accidental acute transmural myocardial infarction during angiography of a 45-year-old man with a history of unstable angina is reported by Baroldi 1995 (194): the occlusion of a coronary artery developed 20 minutes after the occurrance of myocardial ischemia in ECG. A longer citation from Baroldi 1995 (194), p. S 4 “Following the fourth left anterior descending injection, the first ischemic electrocardiographic alteration (downsloped ST) occured. At this time there were no subjective or other clinical signs. Since the ECG abnormality persisted, four successive left anterior descending injections were performed without evidence of any change in the angiographic imagings of the coronary lesions. At the last injection the left anterior descending became fainter and disappeared. Again, this change did not result in any subjective, hemodynamic or clinical modifications. Immediate intracoronary vasodilator followed by calcium-antagonists and urokinase failed to restore the flow. ...At this time (approx. 90 min from the first ischemic ECG) the patient felt mild chest discomfort. Percutaneous transluminal angioplasty was then successfully done with re-establishment of a normal left anterior descending lumen. Paradoxically the clinical pattern deteriorated (increased chest pain and marked ST-elevation). Repeated contrast injections in the left anterior descending artery demonstrated ist progressive disappearance from the distal portion to ist origin from the left main trunk. Since another angioplastic attempt failed to restore flow, the patient underwent coronary artery bypass surgery. At that time, the whole left anterior descending artery was filled with coagulated blood (not thrombus) and the lumen was normal. When the clamp was released, both left anterior descending artery and the implanted vein graft distended but there was no flow indicated by the flow-meter. Repeated probings were unsuccessful. The patient recovered from a large antero-lateral-septal infarct.“

Citation Baroldi 1995 (194), p. S 6: “All the therapeutical procedures and clinical / pathological data apparently excluded the role of a spasm, or thrombus in the intramural system. The angiographic ´occlusion´ progressing from distal to left anterior descending origin (not at the site of previous stenoses) at the bifurcation of the main left trunk (unrestricted flow in the left circumflex branch) attested that hindrance of flow in the left anterior desending artery (and vein graft) was due to intramural blockage with secondary blood coagulation (not thrombosis). One case is one case. However, if the latter is the only case of acute transmural infarct in which the sequence of the events was documented, it raises some justified questions and comments. The first question is how many of the 87 % angiographic occlusions in vivo are pseudo-occlusions. Another question concerns the nature of the material removed at surgery or by atherectomy or seen by angioscopy: thrombus or coagulum ? The layered aspect of the different blood elements favors the latter diagnosis. Unfortunately, thrombus and coagulum (´red thrombus´) are often confused.“

Citation Baroldi 1995 (194), p. S 5: “As far I know, this is the only case in the literature in which several events were monitored. It may help in reviewing and understanding the sequence of physio-pathological mechanisms in the natural history of ischemic heart disease in general and acute coronary syndromes in particular.“ Citation p. S 7: “Two final comments regard: (a) the long period of time (90) min in the reported case, from the first ischemic ECG signs to manifest chest pain. This delay questions the correctness in timing the onset of an infarct in several clinical reports and trials; and (b) the angiographic imaging of thrombosis in atherosclerotic plaque of patients with unstable angina. The hypothesis of recurrent thrombosis plus embolization is contradicted by the previously reported case and, in general by the fact that these plaques may maintain for years their ´irregular´ aspects (195) without relation to clinical course. Several studies have shown that fibrinolytic therapy did not improve the prognosis of these patients (196). The concept of unstable, thrombogenic and emboligenic plaque, as the cause of acute coronary syndromes, still needs to be proven.“ Lange & Hillis 1998 (197) report in the “New England Journal of Medicine“ about four large studies with together more than 6400 patients with unstable angina or myocardial infarction, that investigated the use and overuse of angiography and revascularization for acute coronary syndromes in comparison with a control group that underwent a more conservative, medicinal management with revasularization surgery of only few selected patients. Citation p. 1838: “With remarkable clarity and consistency, all four studies show that routine angiography and revascularization do not reduce the incidence of nonfatal reinfarction or death as compared with the more conservative, ischemia-guided approach. In fact, in the VANQWISH study of patients with non-Q-wave infarction, the aggressive strategy (which those investigators call “invasive“) was associated with increased mortality during hospitalization, at one month, and at one year.“

Citation Baroldi 1995 (194) p. S 8: “Cause and pathogenesis of acute coronary syndromes, and ischemic heart disease are still hypothetical. Data may support an antagonist view according the following concepts (198-199): The coronary thrombus..., the frequency of which may have little, if any significance. In fact - and despite some unproved angiographic findings - the thrombus forms in severe stenosis already by-passed by functioning collaterals (199). Therefore, one may speculate that hemorrhage, rupture of the plaque and thrombosis (never shown in small plaques) are secondary events following an infarct. In the case previously reported the infarct was associated with blockage of intramural flow not due to embolization or ´no reflow´phenomenon, unlikely due to spasm of the intramural arterial vessels, and more probably due to extravascular compression by hyperdistension of atonic myocardium (worsening of preexisting hypokinesis) by intraventricular pressure. This intramural hindrance of flow determined a stasis in the infarct-related artery. When this occurs in a vessel with severe atheromathous and vascularized plaque bypassed by collaterals, hemorrhage and possible spasm leading to secondary fissuration and thrombus formation can be expected. (199). Clinical or experimental angioplasty does not result in thrombosis or severe embolization despite fracture of the wall. ...“ Baroldi 1995 (194) states that atherosclerosis may accelerate when distal intramural perfusion is impaired (increased stress forces on and neurogenic conrol of the arterial wall). Citation of Sroka 2004 (200), p.777: “...as a result of such an ischemia, secondary vascular lesions in the coronary-arterial system can occur. The sudden increase of the peripheral vascular resistance accompanying the onset of myocardial ischemia results in abrupt pressure increases within the supplying artery. In this case, tears in the intima and ruptures of plaques can occur, which then themselves can possibly trigger thromboltic-occlusive vascular processes.“

Baroldi 1998 (185) reports of another interesting finding: Adventitial lympho-plamacellular infiltrates around nerves adjacent to the tunica media at plaque site, may have a role both in the regional myocardial asynergy and / or coronary spasm and may be an important trigger of acute coronary sndrome. This process is only present in coronary ischemic patients.

An alternative generation of ischemia

That there is more than only one access to the complex of ischemia, i.e. the coronary stenosis and lack of oxygen, is documented by the follwoing finding: It is known that L-propionylcarnitine prevents ischemia-induced ventricular dysfunction and ST-segment depression in the ECG, not by affecting the myocardial oxygen supply-demand ratio but as a result of its intrinsic metabolic actions (201). As a (perhaps demagogic) parallel a lack of fuel is not the only possible cause of motor problems. This does not exclude the possibility of different mechanisms (i.e. sufficient or insufficient oxygen supply) existing simultaneously in different myocardial aereas.

Hypothetically (a secondary) ischemia could also be generated by the following cascade of events (which should not take place of the accepted hypothesis of ischemia pathogenesis, but could be a complementary cause of ischemia):

The overstimulation of sympathetic nervous system plays a causal role in cardiac infarction, angina pectoris (196, 202-203) and heart insufficiency (204). The hypersympathetic tone leads to massive glycogenolysis, glucose uptake, glucose oxidation and glycolysis, with only a minimal increase of fatty acid oxidation. The supply of pyruvate exceeding the mitochondrial capacity could lead to severe (areobic) lactate formation in the presence of sufficient amounts of oxygen, an aerobic glycolysis (205-207). The high pyruvate / lactate ratio in the coronary sinus blood of patients with angina pectoris, which are investigated predominantly only in the 1960ies, support this possibility (208-212). In animal models of ischemia due to coronary ligation there is a low pyruvate / lactate ratio (213). In patients with unstable angina pectoris myocardial glucose utilization is enhanced in spite of the absence of clinical, electrocardiographic, or detectable perfusion evidence of acute ischemia (214). In patients with coronary artery disease an acceleration in glucose utilization is visible also in myocardial areas supplied by normal coronary arteries (215).

In this situation of lactate production by aerobic glycolysis the decreased pH together with free radicals originating not only from leucocytes and endothelium but also from myocellular mitochondria (216-218) could inhibit the Na-K-ATPase of erythrocytes and could start the vicious circle described above. The tissue acidification could lead to a decrease in contractility (219-220) with subsequent stretching of the myocardial wall and increase of tissue pressure which also promotes ischemia and stasis in the coronary system (194, 221).

The myocardium, especially the inner, subendothelial layers of the left ventricle, can get supplied with oxygen and all other necessary substances only during the diastole, because during the systole the whole tissue is so compressed that all blood is driven back to more proximal sections. It is obvious that an increased heart rate due to a hyperactivity of the sympathetic nervous system contributes to ischemia not only because of increased demand but also because of diminished nutrition time periods of the myocardium. This leads also to a reduced lactate clearance and further tissue acidification.

In the presence of a functionating parasympathetic nervous system a strong sympathetic stimulation leads to an enhancement of acetylcholine production by about 20 times to counterbalance the sympathetic dominance. Simultaneously, afferent vagal fibers induce a reflex withdrawal of norepinephrine production (222, 223). Together with acetylcholine an effectual NO production leads to an enhancement of cGMP production in the myocardial cell to counterbalance the adrenergic cAMP production. In a healthy heart this measures are sufficient to to reestablish the adrenergic-cholinergic balancing process and have a causal anti-ischemic effect. But in the ischemic heart the sympathetic-vagal balance is badly defective.

The activity of the parasympathetic nervous system is markedly decreased in the minutes before ischemia, in part nearly to zero (200, 224-229, see also 230), as measured by heart rate variability (HRV). This leads in the presence of a preexisting increased sympathetic activity to a catapult-like, excessive overstimulation of sympathetic influence on the heart. The acute withdrawal of vagal drive preceding the onset of ischemia are not dependent on coronary artery disease (231-234).

Acute increases of sympathetic activity alone are mostly of no significance for the onset of ischemia (235).

Citation Sroka 2004 (200) p. 769: “A withdrawal of vagal heart activity previous to any manifestation of coronary artery disease proved to be an independent predictor for the onset of cardiac events in the following years (236)“. Citation p. 771: “The extent of vagal withdrawal in instable angina proved to be a prognostic marker in a study continous vagal withdrawals came along with persistent recurrent ischemic events, and increases of tonic vagal activity along with improvements (237).“ Citation p. 772: “As a result of numerous examinations, the extent of vagal withdrawal within the early post-infarction phase proved to be the strongest predictor for the risk of cardiac death within the following years (238-245).“

Citation Sroka 2004 (200), p. 772: “Until around 30 years ago, the medical profession worked on the principle that vagal innervation of the mammal heart is limited to the atrium. This view has since then been revised. ...The density of the cholinergic innervation of the ventricle is assumed to be approximately one fifth in comparison to the atrium (246). A striking characteristic of the parasympathetic cardiac innervation lies in the neuroeffectoric junction between the cholinergic fiber and the myocardial cell. In this case, there are no typical synapses but the terminal cholinergic fibers form varicosities that release acetylcholine (ACh) into the interstice. ACh diffuses spontaneously over distances of up to many tens of micrometers and thus reaches effector cells within a relatively large area. These facts were described for the first time 1958 (247) and are now proven (246). Due to this special neuroeffectoric junction, the parasympathetic nervous system reaches, despite its low postganglionbic fiber density, all myocardial cells whose cholinergic receptors are randomly distributed over the entire cellular surface (246)."

In the case of a transplanted heart all nerval connections are lacking. The influence of the parasympathetic nervous system is abolished, the blood catecholamines can act without control: there is a massive lactate production, despite excellent perfusion and oxygen supply (248-250).

Citation Sroka 2004 (200) p. 771: “According to the present state of knowledge provided by HRV analysis, roughly three quarters of myocardil ischemic events are triggered by the autonomic nervous system.“

HRV is higher in females, especially before menopause, lower during winter and decreased by physical and mental strain, a sedentary lifestyle and smoking, whereas physical exercise increases tha vagal tone. Citation Sroka 2004 (200), p. 777: “Especially during childhood, HRV analyses have made it clear that a vivid emotional and relational life is of crucial importance for the development of tonic vagal activity. Permitted feelings, emotional expressiveness and the ability to relate strengthen the vagal tone. The suppression of feelings and affects as well as a lacking ability to relate weaken cardiac vagal activity already during childhood. ...Psychological processes apparently influence the central parasympathetic power to a large extent. By means of HRV analysis, it is proven today that the tonic vagal activity is an intregral part of the socio-emotional development of a human being (251). ...Chronic suppression of the expression of feelings weaken the vagal tone (252). .... Touch (253), sex (255) and love (255) stimulate cardiac vagal activity.“

The hypothesis of a noncoronaryly generated ischemia is paralleled by the paradigm shift regarding sepsis, which shows that lactate production by sceletal muscle is not caused by a lack of oxygen, in humans (88, 256-257) and animals (89-90, 99-102, 258-60 nor by a defect in energy production (259-261). The title of the study of Gore et al. 1996 (257) is: “Lactic acidosis during sepsis is related to increased pyruvate production, not deficits in tissue oxygen availability.“ The same mechanism was accepted by Prof. Joseph Keul already in 1967 regarding the skeletal muscle during exercise (261-262). Also Cerretelli & Samaja M2003 (263) speak about an aerobic glycolysis that generates sizeable amounts of lactate and H(+) by way of the excess of glycolytic pyruvate supply.

Only a short notice regarding two points which are widely ignored: Vitamin B1 is a neurotransmitter of the parasympathetic nervous system (synonym: “Aneurin“ !). Furthermore the acetycholine synthesis is dependent of Vit. B1, also the degradation of glucose: Vit. B1 is part of the alpha-carboxylase I, which is necessary for the degradation of pyruvate and the following oxidative steps. Without Vit. B1 only anaerobic glycolysis is possible. It is approximated that the average population in the western world with its generally deficicency of vital substances in the fabrical food has a deficicency of vit. B1 because of the consumation of isolated carbohydrates (white flour and fabrical sugar in all variations).

The other one is the point of “hyperproteinism“, which has been intensively investigated by Prof. Lothar Wendt (Frankfurt on the Main). Too much protein because of a high consumation of meat results in a protein storage in the capillaries and later in the bigger arteries. The basal membran directly behind the endothel cell layer thickenes up to tenfold, and also the pores of this membrane get narrowed. Also the interstice is a target for the protein deposition. The effect is a hindrance of the passage of important substances, for example Vit. B1, a relatively large molecule, and ouabain and carnitine. (Oxygen is a very small molecule !) Also the evacuation of metabolic end products is complicated. According to Prof. Wendt this phenomenon is the cause of essential hypertension, because the organism augments the blood pressure to enforce the hampered passage through the smaller pores of the thickened endothel membrane. Furthermore it triggers atherosclerosis, because this protein deposition boosts the inflammatory processes known to be involved in atherosclerosis.

I think his elaborated books are only available in german language, but I found a reference in Pubmed (264), unfortunately without abstract, and a lot of pages at google about his work, for example:


* About the author

After Rolf-Jürgen Petry had finished his schooling as an alternative practitioner in 1997, he became a permanent visitor of the medical libraries, where he had copied about 20.000 pages in the last years about ouabain and myocardial infarction. He has read many original studies and found that the orthodox positions with which ouabain is rejected exhibit serious faults. It's really a severe miscarriage of medical justice, as you could see with the proofs above.

He has written the first extensive and detailled book on this theme with 1380 references and the preface of Prof. Hans Schaefer from Heidelberg, who was a world-famous physiologist for some decades. The sharp attacks against the oral ouabain therapy by eminently respectable exponents of the medical establishment are described clearly but always objective and without polemics. The book came out in 2003 and the second edition is in process.

Rolf-Jürgen Petry: Die Lösung des Herzinfarkt-Problems durch Strophanthin (The solution for the problem of myocardial infarction), 320 pages text + 40 pages references, 24,90 €
ISBN 3000195874
Verlag Florilegium, Pf 1305, D 27442 Gnarrenburg, Germany
Tel. 0049 - 421 - 59 707 92
Fax 0049 - 1212 - 55 14 09 321
e-mail: strophanthin@web.de

The book is on a high scientific level, but at the same time the author had taken great care that it remains understandable even for a person without previous medical knowledge. This book is available only in German language until now. I am searching for a publishing house for an english transcription...


1) in german: Dohrmann RE & Dohrmann M: Neuere Therapie der instabilen Angina pectoris bei koronarer Herzerkrankung, Erfahrungsheilkunde - acta medica empirica 33: 183-190, 1984
2) in german: Dohrmann RE; H.D.Janisch & M.Kessel: Klinisch-poliklinische Studie über die Wirksamkeit von g-Strophanthin bei Angina pectoris und Myokardinfarkt, Cardiol Bull (Cardiologisches Bulletin) 14/15: 183-187, 1977
3) in german: Dohrmann RE, M.Dohrmann, H.D.Janisch, M.Kessel & H.von Tilly: Senkung der Infarktletalität doch möglich? Ärztliche Praxis 29: 1003-1004, 1977
4) summary in english: Dohrmann RE & Heller RF: Therapeutische Ergebnisse bei akutem Myokardinfarkt unter Anwendung hoch-dosierter Steroidgaben und fluiditätsbeeinflussender Pharmaka - Ergebnisse einer 10-Jahres-Studie, Cardiol Bull 24: 17, 1987
5) in grman: Avenarius HJ, H.Poliwoda & B.Schneider: Unersuchungen zum klinischen Verlauf des akuten Myokardinfarkts. Med Klin 72: 459-464, 1977
6) Prof. Quantiliano de Mesquita, Professor Honorario de Faculdade de Medicina de Universidade Federal de Paraiba. Chefo do Instituto de Angio Cardiologia de Hospital Matarazzo e Cas de Saude Matarazzo Sao Paulo: Teoria miogenico do enfarte miocardio. Verlag: Gemini, Sao Paulo (Brasilien), 1979, in Rundbrief 42 der Int.Gesellschaft für Infarktbekämpfung, Febr.1980, please look to179)
7) in german: Brembach H: Infarktvorbeugung in der Arbeitsmedizin, notabene medici 7: 613-616, 1984
8) in german: Salz H& Schneider B: Perlinguales g-Strophanthin bei stabiler Angina pectoris, Z Allg Med (Zeitschrift für Allgemeinmedizin) 61: 1223-1228, 1985
9) in german: Eine Dokumentation ambulanzkardiologischer Therapie-Ergebnisse nach Anwendung oralen g-Strophanthins, Herbert Pharma GmbH, Wiesbaden, 1984
10) in german: Berthold Kern: Der Myokard-Infarkt. Haug Verlag, Heidelberg (1969), p. 199-203
11) von Ardenne M: Research on the mechanism of myocardial infarctions and on counteracting measures, a new galenic form of the fast acting g-strophanthin, Agressologie 19: 13-22, 1978 (no abstract in PubMed)
12) in german: Hupe H, Balint T: Anwendungs-Untersuchung über die Behandlung pectanginöser Beschwerden mit Strophactiv-Tropfen. Krankenhaus Osterforde (1988); unpublished, for litereature please ask Rolf-Jürgen Petry, Pf. 1305, D 27442 Gnarrenburg
13) Luckhaupt-Koch K: Besonderheiten der Intnsivbehandlung, in W.Dick (Hrsgb.): Notfall- und Intensivmedizin. DeGruyter Lehrbuch, Berlin - N.Y., 1992, p. 436 - 450, on p. 437
14) Bastigkeit M: Medikamente in der Notfallmedizin, Verlagsges.Stumpf & Kossendey, Edewecht, 2001, p.171
15) Repke K: Metabolism of Cardiac Glycosides, in:W.Wilbrandt + P.Lindgren (Eds.): Complete Proceedings of the 1.Int Pharmacol Meeting, Stockholm 1961 Vol III, pp 47-73, Pergamon Press 1963
16) Godfraind T (Brussels): Stimulation and inhibition of the Na+,K+-pump by cardiac glycosides, in Kurt Greeff (ed.): Cardiac Glycosides, Handbook of Experimental Pharmacology Band 56/I, Springer Hdlbg-B-NY 1981, S.381-393
17) Gao J, Wymore RS, Wang Y, Gaudette GR, Krukenkamp IB, Cohen IS, Mathias RT. (New York): Isoform-specific stimulation of cardiac Na/K pumps by nanomolar concentrations of glycosides. J Gen Physiol 119(4): 297-312, 2002
18) Manunta P & Ferrandi M (Milan / Italy): Different effects of marinobufagenin and endogenous ouabain. .J Hypertens 22(2):257-9, 2004 (no abstract in PubMed)
19) Balzan S, D'Urso G, Nicolini G, Forini F, Pellegrino M, Montali U: Erythrocyte sodium pump stimulation by ouabain and an endogenous ouabain-like factor. Cell Biochem Funct 25(3): 297-303, 2007
20) Hambarchian N, Brixius K, Lu R, Muller-Ehmsen J, Schwinger RH (Cologne / Germany): Ouabain increases myofibrillar Ca2+ sensitivity but does not influence the Ca2+ release in human skinned fibres. Eur J Pharmacol. 492(2-3):225-31, 2004
21) Su SW, Wang YL, Li JX, Mei HS, Yin JX (Shijiazhuang / China): Relationship between cardiotonic effects and inhibition on cardiac sarcolemmal Na+,K+-ATPase of strophanthidin at low concentrations. Acta Pharmacol Sin 24: 1103-7, 2003
22) McGarry SJ & Williams AJ: Digoxin activates sarcoplasmatic reticulum Ca++-release channels: a possible role in cardiac inotropy. Br J Pharmacol 108: 1043-1050, 1993
23) Fujino M & Fujino S: An immunohistochemical study of the significance of a new 31,5 kD ouabainreceptor protein isolated from cat cardiac muscle. Jpn J Pharmacol 67: 125-135, 1995
24) Santana LF, A.M.Gomez & W.J.Lederer: Ca++ flux through promiscuos cardiac Na+ channels: slip-mode conductance. Science 279: 1027-33, 1998
25) Horackova M& Mullen S (Halifax,Kanada): The dual effects of ouabain on 45Ca++ transport and contractility in adult rat ventricular myocytes. Pflügers Archiv 412: 277-284, 1988
26) Cross HR, Radda GK, Clarke K: The role of Na+/K+ ATPase activity during low flow ischemia in preventing myocardial injury: a 31P, 23Na and 87Rb NMR spectroscopic study. Magn Reson Med. 1995 Nov;34(5):673-85
27) Bersohn MM (Los Angeles): Sodium pump inhibition in sarcolemma from ischemic hearts. J Mol Cell Cardiol 27: 1483-89, 1995
28) Ko T, Hajime Otani, Hiroji Imamura, Kyoko Omori & Chiyoko Inagaki (Osaka / Japan): Role of sodium pump activity in warm induction of cardioplegia combined with reperfusion of oxygenated cardioplegic solution. Magn Reson Med 34: 673-685, 1995
29) Riehle M and Bereiter-Hahn J (Frankfurt/M. / Germany): Ouabain and Digitoxin as modulators of chick embryo cardiomyocyte energy metabolism. Arzneim-Forsch 44: 943-947, 1994
30) Gousios AG, James M.Felts, Richard J.Havel (San Francisco + Bethesda) 1967 Circ Res 21: 445-448, Effects of ouabain on force of contraction, oxygen consumption, and metabolism of free fatty acids in the perfused rabbit heart. Naunyn-Schmiedebergs Arch Pharmacol 356: 203-209, 1967 (no abstract in PubMed)
31) Peschera A, L.E.Ferrari, E.Arrigoni-Martelli & W.C.Hülsmann (Pomezia / Italien & Rotterdam): Uptake and release of carnitine by vascular endothelium in culture; effects of protons and oxygen free radicals. Mol Cell Biochem 142: 99-106, 1995.
32) Bartels L, W.J.Remme & H.R.Scholte (Rotterdam): Acute myocardial ischaemia induces cardiac carnitine release in man. Eur Heart J 18: 84-90, 1997
33) Sharma VK, Lorelle A.Pottick & Shailesh Banerjee (New York): Ouabain stimulation of noradrenaline transport in guinea pig heart. Nature 286: 817-819, 1980
34) Gutman Y& Boonyaviroj P: Mechanism of inhibition of catecholamine release from adrenal medulla by diphenylhydantoin and by low concentration of ouabain (10 (-10) M). Naunyn-Schmiedebergs Arch Pharmacol 296: 293-296, 1977
35) Agostoni PG, Elisabetta Doria, Marco Berti & Maurizio D.Guazzi (Milan / Italy): Long-term use of k-strophanthin in advanced congestive heart failure due to dilated cardiomyopathy: a double-blind crossover evaluation versus digoxin. Clin Cardiol 17: 536-541, 1994
36) Branco D& Osswald W: Ouabain-induced efflux of catecholaminess and metabolites from blood vessels of
normotensive and hypertensive dogs, in E.Erdmann, K.Greeff, J.C.Skou: Cardiac Glycosides 1785-1985, Steinkopff Verlag, Darmstadt, 1986
37) Lopez JA, Timmis AD, Garan H, Homcy CJ, Powell WJ Jr. (Boston / USA).: Effect of intracarotid administration of ouabain in dogs. Am J Physiol 254:H148-H155, 1988
38) Joubert HB: Effects of cardiac glycosides on autonomic nervous system and endocrine glands. In: Greeff K (Hrsg.): Cardiac Glycosides. Handbook of Exp Pharmacol, Band 56 I. Springer (1981), S. 533-550
39) L'Abbate A: Recanalization versus reperfusion for myocardial survival and preservation of ventricular geometry. Am Heart J 138:S89-S95, 1999
40) Heusch G, Deussen A, Thamer V.: Cardiac sympathetic nerve activity and progressive vasoconstriction distal to coronary stenoses: feed-back aggravation of myocardial ischemia. J Autonomic Nerve System 13:311-326 (1985)
41) Matsumori A, Koh Ono, Ryosuke Nishio, Hiseki Igata, Tetsuo Shioi, Shigeo Matsui, Yutaka Furukawa, Atsushi Iwasaki, Yoshisuke Nose, Shigetake Sasayama (Kyoto / Japan): Modulation of cytokine production and protection against lethal endotoxemia by the cardiac glycoside ouabain. Circulation 96: 1501-6, 1997
42) Qi SS et al.: Clinical evaluation of intermittent strophanthin K therapy for congestive heart failure combined coronary artery disease. (article in chinese, abstract in english) Hunan Yi Ke Da Xue Xue Bao 26:448-450, 2001
43) in german: Berthold Kern: Der Myokard-Infarkt. Haug Verlag, Heidelberg (1969), p. 122 ff.
44) in german: Kracke R: Zur perlingualen Strophanthin-Therapie. Dtsch Med Wschr 79:81-83, 1954
45) Pidgeon GB, Richards AM, Nicholls MG, Lewis LK, Yandle TG. (Christchurch / New Zealand): Acute effects of intravenous ouabain in healthy volunteers. Clin Sci (Lond). 1994 Apr;86:391-397, 1994
46) DeMots H, Shabudin H.Rahimtoola, John H.McAnulty, George A.Porter (Portland / USA): Effects of ouabain on coronary and systemic vascular resistance and myocardial oxygen consumption in patients without heart failure, Am J Cardiol 41: 88-93, 1978 (No abstract available at PubMed)
47) in german: Saradeth T & Ernst E (Vienna): Hämorheologische Effekte durch g-Strophanthin, Erfahrungsheilkunde 40: 775-776, 1991
48) in german: v.Ardenne M, W.-K. Mayer, J.Schmidt, G.Rostock & W.Mohnike (Dresden): Klinische Prüfung des perlingual applizierten g-Strophanthin-Präparats Strodival® spezial mit Hilfe der 99 mTc-MyospectHerztomographie. Z Klin Med 46: 667-669, 1991
49) Vatner SF & H.Baig (Harvard): Comparison of the effects of ouabain and isoproterenol on ischemic myocardium of conscious dogs. Circulation, 58: 654, 1978 (No abstract available at PubMed)
50) Murphy JR: The influence of pH and temperature on some physical properties of normal erythrocytes anderythrocytes from patients with hereditary sphenocytosis. J Lab Clin Med 69: 758-775, 1967
(No abstract available at PubMed)
51) Schmid-Schönbein H, E.Volger, J.Weiss & M.Brandhuber: Effect of 0-(ß-hydroxyethyl)-Rutosides on the microrheology of human blood under defined flow conditions. Vasa 4: 263-270, 1975
(No abstract available at PubMed)
52) Tsuda K, Hiroki Shima, Keizo Kimura, Ichiro Nishio & Yoshiaki Masuyama (Wakayama / Japan): Effects of ouabain on membrane fluidity of erythrocytes in essential hypertension. An electron spin resonance study. J Hypertens 4: 783-785, 1991
53) in german: Strobelt W, U.Karsten, W.Lohmann (Giessen): Biophysikalische Untersuchungen an Erythrocyten mit äquivalenten Dosen von g-Strophantin perlingual und Digitoxin zur Frage der Flexibilität und Mikroperfusion, Rundbrief 68 (April 1986) der Internat. Gesellschaft für Infarktbekämpfung, Schorndorf
54) Murakami T, Sumio Mizuno, Yoshifumi Takahashi, Kazuo Ohsato, Ikuo Moriuchi, Yoshiyuki Arai, Junichira Mitune, Masami Shimizu & Maseratu Ohnaka (Kanazawa / Japan): Intracoronary aspiration thrombectomy for acute myocardial infarction. Am J Cardiol 82: 839-844, 1998
55) Gertz SD, Kragel AH, Kalan JM, Braunwald E, Roberts WC: Comparison of coronary and myocardial morphologic findings in patients with and without thrombolytic therapy during fatal first acute myocardial infarction. The TIMI Investigators. Am J Cardiol. Oct 15;66(12):904-9, 1990
56) Silver ML, G.Baroldi & F.Mariani: The relationship between acute occlusive coronary thrombi and myocardial infarction study in 100 consecutive patients. Circulation 61: 219-227, 1980 (No abstract available at PubMed)
57) Baroldi G: Coronary thrombosis: facts and beliefs. Am.Heart J. 91: 683-688, 1976 (No abstract available at PubMed)
58) Baroldi, G. et al.: Morphology of acute myocardial infarction in relation to coronary thrombosis. Am Heart J 87: 65, 1974 (No abstract available at PubMed)
59 a) Roberts, W.C. and Buja, L.M. :The frequency and significance of coronary arterial thrombi and other observations in fatal acute myocardial infarction. A study of 107 necropsy patients. Am J Med 52: 425-443, 1972 (No abstract available at PubMed)
59 b) Summary of 134 a) on p. 827 in: A.B.Chandler et al.: Special report: Coronary thrombosis in myocardial infarction, report of a workshop on the role of coronary thrombosis in the pathogenesis of acute myocardialinfarction. Am J Cardiol 34: 823-833, 1974 (No abstract available at PubMed)
60) Baroldi, G.: Functional morphology of the anastomotic circulation in human cardiac pathology. Methods Arch Exp Pathol 5: 438-473, 1971 (No abstract available at PubMed)
61) Baroldi.G and Scomazzoni.G: Coronary circulation in the normal and pathologic heart, American registry of Pathology, Armed Forces Institute of Pathology, Government Printing office. Washington,1967
62) Baroldi, G.: Acute coronary occlusion as a cause of myocardial infarct and sudden coronary heart death. Am J Cardiol 16: 859-880, 1965 (No abstract available at PubMed)
63) Ehrlich, J.C. & Shinohara, Y.: Low incidence of coronarythrombosis in myocardial infarction. Arch. Pathol. 78: S.432, 1964 (No abstract available at PubMed)
64) Spain DM& Bradess VA (N.Y.): The relationship of coronary thrombosis to coronary atherosclerosis and ischemic heart disease. Am.J.Med.Sci. 240: 701, 1960 (No abstract available at PubMed)
65) in german: Doerr W, Höpker WW, Roßner JA: Neues und Kritisches vom und zum Herzinfarkt. Sitzungsbericht der Heidelberger Akademie der Wissenschaften math.-nat.Klasse. Springer, Berlin, Heidelberg, New York, 1974
66) in german: Popper, L. und Feiks, F.K.: Herzinfarkt und Koronarthrombose. Wiener Klin.Wschr. 73: 421, 1961
67) Pidgeon GB, A.M.Richards, M.G.Nicholls, C.J.Charles, M.T.Rademaker, K.L.Lynn, R.R.Bailey, L.K.Lewis & T.G.Yandle (Christchurch / Neuseeland): Chronic ouabain infusion does not cause hypertension in sheep. Am J Physiol 270: E 386-E 392, 1996
68) Pidgeon GB, Richards AM, Nicholls MG, Lewis LK, Yandle TG. (Christchurch / New Zealand): Acute effects of intravenous ouabain in healthy volunteers. Clin Sci (Lond) 1994 Apr;86: 391-397, 1994
69) in german: Kubicek F, Th.Reisner: Hypoxietoleranz bei koronarer Herzkrankheit unter der Einwirkung von Digoxin, ß-methyl-Digoxin und g-Strophanthin, Ther d.Gegenw (Therapie der Gegenwart) Heft 5 1973, S.747-768
70) Sharma B, P.A.Majid, M.K.Meeran; W.Whitaker & S.H.Taylor (Leeds / GB): Clinical, electrocardiographic, and haemodynamic effects of digitalis (ouabain) in angina pectoris. Br Heart J 34: 631-637, 1972
Free full text at
71) Belz GG, J.Mathews, U.Sauer, H.Stern & B.Schneider (Wiesbaden /Germany): Pharmacodynamic effects of ouabain following single sublingual and intravenous doses in normal subjects. Eur J Clin Pharmacol 26: 287-292, 1984
72) summary in english: Dohrmann RE und Schlief-Pflug E (Berlin): Echokardiographische Studie zum Wirkungsnachweis äquivalenter Dosierungen von Nitrolingual und Strodival spezial bei Patienten mit koronarer Herzkrankheit Cardiol.-Angiol Bull 23: 18-22, 1986
73) Aceto E, Vassalle M: On the mechanism of the positive inotropy of low concentrations of strophanthidin. J Pharmacol Exp Ther 259:182-189, 1991
74) Piscitello F & Maggi GC: Effectiveness of orally administered g-Strophanthin on haemodynamics in cardiac patients, Arzneim.-Forsch (Drug Res) 23: 1546-1547, 1973 (No abstract available at PubMed)
75) in german: Moskopf E & Dietz H: Experimentelle u. klinische Untersuchungen über eine zuverlässige orale Strophanthintherapie. Die Medizinische Welt 1955, p. 1375-77
76) summary in english: Heiss WD, Reisner T, Reisner H, Havelec L, Kubicek F & Dietmann K (Wien): Effect of ouabain on cerebral blood flow, Wiener klinische Wochenschrift 88: 171-174, 1976
77) in german: Birkmayer W et al.(Wien): Der cerebrale Nutritionseffekt im Isotopenangiogramm. Archiv für Psychiatrie und Zeitschrift f.d. gesamte Neurologie (1961), p. 346-353
78) Agrawal KP, Charles E.Reed, Robert E.Hyatt, Wayne E.Imber, Willane S.Krell: Airway responses to inhaled ouabain in subjects with and without asthma. Mayo Clin Proc 61: 778-784, 1986
79) abstract in english, article in german: Michalik M, R.Uebelhack, I.Grote, G.Ehle & K.Seidel: [Vegetative parameters under the effect of ouabain (g-strophanthin) in endogenous depressive patients. 1. The salivation rate] Schweiz Arch Neurol Neurochir Psychiatr 125: 163-178, 1979
80) Hsieh CC, Hwang TL, Chen HM, Chen MF, Sun YF, Lau YT (Taipeh / Taiwan): Sepsis correlated with increased erythrocyte Na+ content and Na+ - K+ pump activity. J Biomed Sci. 10(4):389-95, 2003
81) Suri M, L.Kumar, G.Kaur, S.Singhi & R.Prasad (Chandigarh / Indien): Electrolyte disturbances due to ouabain sensitive sodium potassium pump in erythrocytes of children with sepsis. Indian J Med Res 105: 67-71, 1997
82).Schornack PA, Song SK, Hotchkiss R, Ackerman JJ (St.Louis / USA): Inhibition of ion transport in septic rat heart: 133Cs+ as an NMR active K+ analog. Am J Physiol 272: C1635-41, 1997
83) Okamoto K, Wang W, Rounds J, Chambers E, Jacobs DO: Sublytic complement attack increases intracellular sodium in rat skeletal muscle. Surg Res 90(2):174-82, 2000
84) Karlstad MD & Mohammed M.Sayeed: Effect of endotoxin shock on basal and insulin-mediated Na-K-pump activity in rat soleus muscle. Circul Shock 38: 222-227, 1992
85) Liaw KY, L.L.Kuo, C.C.Chen & S.Y.Lin-Shiau: Alteration of Na-K-ATPase, Ca-ATPase and Mg-ATPase activitiy in erythrocytes, muscle and liver of traumatic and septic patients. Circ Shock 22: 195-203, 1987
86) Liu MS& S.Ghosh (St.Louis / ÙSA): Myocardial sodium pump activity in endotoxin shock. Circ Shock 19: 177-184, 1986
87) Tang C, Hsu HK, Chen XY, Liu MS (St.Louis / USA): Externalization and internalization of (Na+ + K+)-ATPase in rat heart during different phases of sepsis. Circ Shock 41: 19-25, 1993
88) Levy B, Gibot S, Franck P, Cravoisy A, Bollaert PE: Relation between muscle Na+K+ ATPase activity and raised lactate concentrations in septic shock: a prospective study. Lancet 365(9462):871-5, 2005
89) Luchette FA, Jenkins WA, Friend LA, Su C, Fischer JE, James JH: Hypoxia is not the sole cause of lactate production during shock. J Trauma. 52: 415-9, 2002with a comment in: J Trauma. 53: 807-8, 2002
90) Luchette FA, L.A.Friend, C.C:Brown, R.K.Upputuri & J.H.James: Increased skeletal muscle Na+, K+-ATPase activity as a cause of increased lactate production after hemorrhagic shock. J Trauma 44: 796-801, 1998
91) v.Ardenne M & Rieger F: Theoretische und experimentelle Grundlagen zur außergewöhnlichen Pharmakokinetik des g-Strophanthin. Arzneimittel-Forschung 22: 1845-53, 1972, see also 11) (Review in english)
92) von Ardenne M & Kern B: Der Herzinfarkt als Folge der lysosomalen Zytolyse-Kettenreaktion, a) in: Heinz Herbert Schöffler (Ed.): Myokardinfarkt, 9.Jahrestagung der Gesellschaft für Infarktbekämpfung 1978, A.W.Gentner Verlag, Stuttgart, 1980 b) in: Dtsch.Gesundheitswesen 26: 1769-1780, 1971, see also 11) (Review in english)
93) in german: Loll H & Blumberger KJ: Änderung des Serumspiegels von Intermediärprodukten und Enzymen durch k-Strophanthin. Ärztl Forsch 14: I/181-I/185, 1960
94) in german: Renk H: Vergleichende Untersuchung über das Verhalten des Milchsäurespiegels bei der Therapie der Herzinsuffizizienz. Med Klin 54: 13-16, 1959
95) in german: Vogel G: Das Adenylsäuresystem im Blut des Herzkranken. Klin Wschr 36: 979-982, 1958
96) in german: Ullsperger R: Pharmazie 9: 330, 1954, in 124)
97) in german: von Blumencron W: Über die Wirkung von Strophanthin und Digitoxin auf den Milchsäurestoffwechsel des Herzens. Klin Wschr. 20: 737, 1941
98) in german: Gollwitzer-Meier, K.: Über die Reaktionsänderungen im Herzen während der Belastung, bei Herzinsuffizienz und unter dem Einfluß von Strophanthin. Pflügers Archiv 245 : 385, 1941
99) McCarter FD, S.R.Nierman, J.H.James, L.Wang, J.K.King, L.A.Friend & J.E.Fischer (Cincinatti / USA): Role of skeletal muscle Na+-K+-ATPase activity in increased lactate production in sub-acute sepsis. Life Sci 70(16): 1875-1888, 2002

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