内皮素对缺氧肝脏的损伤作用及降钙素基因相关肽的拮抗效应

POSSIBLE ANTAGONISM BETWEEN ENDOTHELIN AND CALCITONIN GENE-RELATED PEPTIDE ON HYPOXIC LIVER

本实验在大鼠肝脏原位缺氧灌流模型上,发现10^(-8)mol/L内皮素(ET)灌流,不仅强烈收缩门静脉血管,而且明显加重组织缺氧损伤:加重肝脏水肿、增加组织脂质过氧化物生成和溶酶体酶漏出。应用10^(-8)mol/L降钙素基因相关肽(CGRP)与ET同时灌流,有效地拮抗了ET对缺氧肝脏的损伤作用。

On the hypoxic perfusion model of in situ rat liver, we observed that 10^(-8) mol/L endothelin (ET)exerted a severe vasoconstrictor effect on the portal venous vasculature and significantly augmented thetissue hypoxic damage: augmentation of liver edema, increased production of lipid peroxidation productand leakage of lysosomal enzyme. When 10^(-8) mol/L calcitonin gene-related peptide (CGRP) was addedtogher with ET to the perfusion fluid, it effectively antagonized the damaging effect of ET on thehypoxic liver. The possible pathophysiologic significance of ET and CGRP on hypoxia or anoxia as apathologic process is discussed.