RESUMO
The authors examined the contribution of lipid peroxidation (LPO) in the pathogenesis of hepatic damage in visceral and ischemic shock (VIS) induced by upper mesenteric artery occlusion followed by stepwise revascularization. There was generation of initial and terminal PLO products in hepatic tissue, which increased as VIS and toxemia progressed. The accumulation kinetics of thiobarbituric acid-positive agents in the hepatic homogenates, microsomes, and mitochondria isolated in different periods of VIS was studied. The findings confirm the hypothesis that oxygen radicals play a role in the development of disturbances typical of those in the liver during the shock.
Assuntos
Isquemia/fisiopatologia , Peroxidação de Lipídeos/fisiologia , Hepatopatias/fisiopatologia , Choque/fisiopatologia , Vísceras/irrigação sanguínea , Animais , Isquemia/complicações , Hepatopatias/etiologia , Masculino , Coelhos , Choque/complicaçõesRESUMO
Patterns of lipid peroxidation, chemoluminescence and antiradical activity of rat blood serum were studied after simulation of visceral-ischemic shock developed as a result of two-hour-long ischemia of the small intestines and of right-side part of large intestine. Toxic effects of oxygen, accompanied by considerable activation of lipid peroxidation, were of importance in pathogenesis of this shock. Accumulation of lipid peroxidation products in blood occurred at the step of the intestine ischemia and was distinctly increased after restoration of circulation in the tissue. Increased inhibition of blood serum chemoluminescence as well as elevation of lipid antiradical activity were observed depending on steps of the shock development.