[Role of endothelin-nitrogen monoxide equilibrium in ischemia/reperfusion damage of the liver].
Elevated levels of endothelin (ET) are measured during ischemia and reperfusion, but no adequate increase of nitric oxide (NO) can be observed. Thus, the balance of both substances, which occurs under physiological conditions and regulates microcirculatory vessel widths, is disturbed. This leads to microcirculatory damages. As well ET receptor blocking using a mixed ET receptor antagonist as increase of NO production after L-arginine treatment influenced this pathomechanism. The preischemic sinusoidal diameters were maintained and leukocyte endothelial interactions reduced. Concomitantly, sinusoidal perfusion rate and local hepatic tissue pO2 were increased. Because of significant reduced hepatocellular damage in both therapy groups both therapeutical ways might exert beneficial effects to attenuate ischemia/reperfusion induced microvascular and tissue injury.
D000818:Animals; D016232:Endothelins / Q000502:physiology*; D005260:Female; D007511:Ischemia / Q000503:physiopathology; D008099:Liver / Q000098:blood supply*; D008833:Microcirculation / Q000503:physiopathology; D009569:Nitric Oxide / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000503:physiopathology*; D014655:Vascular Resistance / Q000502:physiology
D016232:Endothelins; D009569:Nitric Oxide