Cytokines and growth factors in endothelial dysfunction.
OBJECTIVE
The purpose of this focused review is to call attention to the important interrelationships between growth factors (e.g., transforming growth factor-beta) and cytokines (e.g., tumor necrosis factor [TNF]) on endothelial function as characterized by the ability of the endothelium to release endothelium-derived relaxing factor.


METHODS
Myocardial ischemia followed by reperfusion leads to a severe degree of endothelial dysfunction characterized by an impaired vasodilator response to endothelial-dependent vasodilators. The reduction in endothelial-dependent responses occurs rapidly after the onset of reperfusion. Endothelial dysfunction was studied in coronary artery as well as superior mesenteric artery rings, and the effects of cytokines, transforming growth factor-beta, and free radicals were assessed.


RESULTS
Oxygen-derived free radicals (i.e., superoxide anion) and cytokines (i.e., TNF) contribute to this endothelial dysfunction, which is characterized by a loss of endothelium-derived relaxing factor, now known to be identical to nitric oxide. Agents such as superoxide dismutase or transforming growth factor-beta can significantly preserve endothelial integrity during ischemia-reperfusion states.


CONCLUSIONS
Endothelial dysfunction is an early and critical phenomenon occurring in ischemia-reperfusion injury both in the coronary and the mesenteric circulations.
Lefer
A M
AM
Department of Physiology, Jefferson Medical College, Thomas Jefferson University, Philadelphia, PA 19107.
Ma
X L
XL
D000818:Animals; D003326:Coronary Circulation / Q000502:physiology; D016207:Cytokines / Q000502:physiology*; D004730:Endothelium, Vascular / Q000378:metabolism / Q000503:physiopathology*; D006133:Growth Substances / Q000502:physiology*; D009569:Nitric Oxide / Q000096:biosynthesis; D015427:Reperfusion Injury / Q000503:physiopathology; D013152:Splanchnic Circulation / Q000502:physiology
D016207:Cytokines; D006133:Growth Substances; D009569:Nitric Oxide