PARACRINE REGULATION OF CARDIAC MYOCYTES IN NORMAL AND SEPTIC HEART

A paracrine pathway for the regulation of cardiac contractile function by nonmuscle cells is documented in the heart. Coronary and endocardi al endothelium release several diffusible agents, such as prostaglandi ns, endothelin-1, and nitric oxide, with an action on cardiac myocyte function. Cardiac diseases involving an immune or inflammatory mechani sm, such as endotoxic shock, are now seen as conditions in which cross -talk between different cell types in the heart is clearly implicated. The potential biological relevance of inducible nitric oxide synthase in the myocardium, and the subsequent production of nitric oxide has been proposed as a mechanism of the cardiac depression observed in sep tic shock. In addition to cardiac myocytes, activated microvascular en dothelial cells and cardiac endothelial cells may contribute to nitric oxide generation and, ultimately, to the depression of myocardial con tractile activity during sepsis. This article reviews the local interc ellular communication between cardiac myocytes and endothelial cells i n the normal heart and discusses some of the mechanisms potentially cl aimed to depress heart function in sepsis. Copyright (C) 1998 by W.B. Saunders Company.