Role of EDRF/NO in Chronic High Coronary Blood Flow States During Myocardial Dysfunction and Failure

  • Thomas H. Hintze
  • Jie Wang
  • Nahid Seyedi
  • Michael S. Wolin
Part of the Clinical Physiology Series book series (CLINPHY)

Abstract

Historically, the changes in cardiovascular function and particularly those that occur in the heart during the development of heart failure have been attributed to alterations in the contractile state of the myocardium (4, 68). Thus either chronic pressure or volume overload are characterized by a reduced inotropic state as shown in papillary muscles removed from failing hearts (77, 78), reduced cardiac contractile indices in experimental animals in vivo (73), and reduced ejection fraction or other measures of myocardial contractility in man (4). At the cellular level, there may be disruption of mitochondria, disarray of myofilaments, focal or diffuse ischemic lesions, concentric or eccentric hypertrophy, depending upon the cause of the myocardial dysfunction (50). This large body of evidence has suggested that the primary insult in heart failure of various etiologies is an alteration in contractile function due primarily to myocyte dysfunction (77, 78). In fact, one of the most active areas of recent investigation is the use of relaxation indexes to uncover diastolic dysfunction in the hope of early detection of potential functional abnormalities in the myocardium (29). All of the above underscore the emphasis on the contractile failure of the myocardium as the progenitor of heart failure.

Keywords

Adenosine Arginine Prostaglandin Norepinephrine Hull 

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© American Physiological Society 1995

Authors and Affiliations

  • Thomas H. Hintze
  • Jie Wang
  • Nahid Seyedi
  • Michael S. Wolin

There are no affiliations available

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