title: Paracrine regulation of cardiac myocytes in normal and septic heart.
abstract: A paracrine pathway for the regulation of cardiac contractile function by nonmuscle cells is documented in the heart. Coronary and endocardial endothelium release several diffusible agents, such as prostaglandins, endothelin-1, and nitric oxide, with an action on cardiac myocyte function. Cardiac diseases involving an immune or inflammatory mechanism, 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 septic shock. In addition to cardiac myocytes, activated microvascular endothelial cells and cardiac endothelial cells may contribute to nitric oxide generation and, ultimately, to the depression of myocardial contractile activity during sepsis. This article reviews the local intercellular communication between cardiac myocytes and endothelial cells in the normal heart and discusses some of the mechanisms potentially claimed to depress heart function in sepsis.
authors.affiliation: Department of Anesthesiology and Intensive Care, IFR Circulation Lariboisière, Hôpital Lariboisière, Paris, France.
authors.forename: S
authors.initials: S
authors.lastname: Corda
authors.forename: A
authors.initials: A
authors.lastname: Mebazaa
authors.forename: B
authors.initials: B
authors.lastname: Tavernier
authors.forename: M B
authors.initials: MB
authors.lastname: Ayed
authors.forename: D
authors.initials: D
authors.lastname: Payen
mesh_terms: D004727:Endothelium; D006801:Humans; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism*; D009569:Nitric Oxide / Q000378:metabolism; D019899:Paracrine Communication; D018805:Sepsis / Q000378:metabolism*
chemical_list: D009569:Nitric Oxide