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Cytokines and Reperfusion Injury
Author(s) -
Nosé Peter S.
Publication year - 1993
Publication title -
journal of cardiac surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.428
H-Index - 58
eISSN - 1540-8191
pISSN - 0886-0440
DOI - 10.1111/j.1540-8191.1993.tb01329.x
Subject(s) - medicine , nitric oxide , reperfusion injury , contractility , tumor necrosis factor alpha , proinflammatory cytokine , intracellular , inflammation , cell adhesion molecule , endothelial stem cell , nitric oxide synthase , endocrinology , pharmacology , ischemia , immunology , microbiology and biotechnology , biology , biochemistry , in vitro
A bstract Myocardial dysfunction following prolonged ischemia and reperfusion is at least partially dependent upon adhesion of neutrophils to myocardial and endothelial cells. Neutrophils are thought to contribute to reperfusion injury by two mechanisms: impairment of the microvasculature by physical obstruction, and secretion of products that damage microvasculature and myocardium. Cytokines have been shown to play several roles in neutrophil aggregation. Interleukin‐6 (IL‐6), along with IL‐1 and tumor necrosis factor‐alpha (TNF‐alpha), induces the expression of intracellular adhesion molecule‐1 (ICAM‐1) in myocytes and endothelial cells, respectively. These cytokines also inhibit contractility and nitric oxide release (a vasodilator), and IL‐1 and TNF‐alpha have been found to reduce adrenergic stimulation of myocardial contractility by reducing intracellular cyclic AMP levels and uncoupling adenylate cyclase from beta receptors. The transforming growth factors, TGF‐alpha and TGF‐beta, also have a role in reperfusion injury. TGF‐alpha reduces endothelial cell release of nitric oxide, while TGF‐beta appears to protect against reperfusion injury by reducing plasma TGF‐alpha levels, blocking neutrophil adherence, and promoting nitric oxide release. Although cytokines are likely to have important roles in reperfusion injury, their involvement in myocardial stunning is unclear.