[Involvement of oxygen-depending processes in the pathogenesis of hepatic reperfusion injury].
The disbalance between reactive oxygen species generation and antioxidant defensive factors importantly contributes in the development of hepatic reperfusion damage. Changes in blood oxygen transport during hepatic ischemia/reperfusion are involved in its development. Ischemia-induced oxyhemoglobin dissociation curve shift rightwards also exists during the hepatic reperfusion and thereby may facilitate the free radical attacks against the liver. The least disorders in blood oxygen transport, prooxidant-antioxidant balance and hepatic morpho-functional state were observed during the postischemic period under the conditions of moderate hypoxia. The protective effect of L-arginine during the hepatic ischemia-reperfusion may be partially due to the changed hemoglobin function and thereby tissue oxygen delivery and to the keeping of body prooxidant-antioxidant balance. The development of new pharmacological tools to modify the blood oxygen transport and generate the optimal nitric oxide amounts may be a promising strategy for correction of reperfusion injury.
Zinchuk
V V
VV
Khodosovskiĭ
M N
MN
D000818:Animals; D001120:Arginine / Q000494:pharmacology; D006801:Humans; D000860:Hypoxia / Q000473:pathology; D008099:Liver / Q000098:blood supply / Q000503:physiopathology; D008102:Liver Circulation / Q000187:drug effects; D008107:Liver Diseases / Q000503:physiopathology*; D010100:Oxygen / Q000008:administration & dosage / Q000097:blood / Q000378:metabolism*; D010108:Oxyhemoglobins / Q000378:metabolism; D015427:Reperfusion Injury / Q000503:physiopathology*
D010108:Oxyhemoglobins; D001120:Arginine; D010100:Oxygen