Drug – bio-affecting and body treating compositions – Designated organic active ingredient containing – Having -c- – wherein x is chalcogen – bonded directly to...
Patent
1995-02-28
2000-05-23
MacMillan, Keith D.
Drug, bio-affecting and body treating compositions
Designated organic active ingredient containing
Having -c-, wherein x is chalcogen, bonded directly to...
514258, 514465, 514704, 514742, 514929, A61K 3144
Patent
active
060666498
DESCRIPTION:
BRIEF SUMMARY
The invention relates to a drug for cardiovascular diseases, in particular dysrhythmia, cardiac insufficiency, myocardial ischemia, angina pectoris and high blood pressure (hypertension), which contains a specific inhibitor, and the application of the specific inhibitor.
Cardiovascular diseases belong to the main reasons for death in the industrialized countries. If the heart is no longer capable of producing an output corresponding to the requirements, i.e. if it no longer has the strength to pump the amount of blood, corresponding to the venous supply, into the circulatory periphery, one talks about a cardiac insufficiency. In so doing, one distinguishes, according to the section of the heart that is affected, between a right ventricular insufficiency, a left ventricular insufficiency and a bilateral insufficiency (global insufficiency), depending on the degree of severity an insufficiency at rest or exercise. A cardiac insufficiency can have mechanical or biochemical causes. A mechanically induced cardiac insufficiency is possible due to long-term overloading of the myocardium as a consequence of increased resistance in the general or lesser circulatory system (e.g. for chronic lung diseases, mitral or aortic stenosis, hypertension), due to the lack of heart muscle fibers associated with myocarditis or heart infarction, dysrhythmia (tachycardia, bradycardia) or due to an obstruction of the heart activity owing to constrictive pericarditis or pericardial tamponade. A biochemically induced cardiac insufficiency occurs when there is a lack of substrate in the heart muscle following inadequate circulation of the blood flow (coronary insufficiency) or disturbed diffusion from the capillaries into the muscle fibers (e.g. with myocarditis) and due to insufficient conversion of chemical energy into mechanical energy as a consequence of a disordered electrolyte or metabolism (shift in K/Ca quotient, lack of vitamin B.sub.1, diabetes mellitus).
The primary goal of drug therapy for cardiac insufficiency is to economize the work of the heart and to raise the contraction strength of the heart muscle fibers.
In so doing, cardiac irregularities, from which young persons can suffer, but which are especially typical in older persons, deserve special attention. The pathological changes underlying cardiac irregularities are based on a disturbance in the formation of excitation and/or a disturbance in the conduction. At the same time the heart rate can be too high (tachycardia), too low (bradycardia) or irregular (arrhythmia).
Ventricular fibrillation is often the cause of sudden cardiac death. In the genesis of such arrhythmias biochemical factors are becoming increasingly more important. However, the exact origin of ventricular fibrillation remains speculative; and to date there still does not exist an effective therapy with drugs. According to one hypothesis, the local concentration of calcium ions released from the heart is associated with the start of arrhythmias and ventricular fibrillation, but the loss of calcium ions and the ventricular fibrillation is sometimes unrelated. It has been proposed that cyclic adenosine monophosphate, the second messenger of cateocholamine activity, is related to the start of ventricular fibrillation.
Therefore, physiological mechanisms, which regulate the synthesis or decomposition of cAMP in ischemic cells, should be significant for the development of a drug for ventricular fibrillation (T. Podzuweit, W. F. Lubbe and L. H. Opie, Lancet i, 341-342, 1976).
In the case of pigs it has been found that early ventricular arrhythmias and ventricular fibrillation, induced by occlusions of the coronary arteries, correlate to increased levels of myocardial cAMP and adenosine. In addition, a relation between the cAMP and adenosine content of ischemic myocardium and the frequency of reperfusive ventricular fibrillation has been proven. Ventricular fibrillation, induced by the proximal occlusion of the Ramus inter ventricularis anterior (Riva) of the left coronary artery, was not hindered by pretr
REFERENCES:
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Database MEDLINE on STN Koke et al, "Inhibitors of adenosine catabolism improve recovery of dog myocardium after ischemia", Molecular and cellular Biochemistry, 86(2) 107-13, Apr. 11, 1989.
Database Chemical Abstracts on STN, Wu et al, "Contractility, ATP, and creatine phosphate during myocardial ischemia and reperfusion . . . ", Cytobios, 50(200), 7-12, Jan. 1987.
MEDLINE Abstract, AN 76138485, Epstein et al, Mar., 1976.
MEDLINE Abstract, AN 91005785, Zhu, Apr., 1990.
Trapani et al, "Hemodynamic Basis for the Depressor Activity of Zaprinast, a Selective cGMP Phosphodiesterase Inhibitor", J. Pharm. & Exp. Therap., vol. 28, No. 1, pp. 269-274, Apr. 09, 1991.
Harris et al, "Phosphodiesterase inhibition and the potentation by zaprinast . . . ", J. Phar.&Exp. Therap., vol. 249, No. 2, pp. 349-400, Jan. 23, 1989.
MacMillan Keith D.
Podzuweit Thomas
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