Ischemic damage of the liver. Part I: In vitro investigation of the prevention of the ischemic lesion of the liver.
In an isolated rat liver perfusion system the effects of normothermal ischemia on hepatic functions were investigated. After 30 minutes of anoxy bile production and BSP elimination capacity of the liver are significantly reduced. The quantity of secreted "ascites" from the surface of the liver several times high after anoxic damage, while oxygen consumption, portal venous pressure and ammonia elimination do not differ significantly from the controls. Pretreatment with insulin plus glucose, isoproterenol, hypoxanthine, chlorpromazine and glucagon (5 micrograms/100 g i.v., or 0.2 mg/100 g s.c.) does not reduce noticeably the normothermal anoxic lesion of the liver Glucagon (50 micrograms/100 g i.v.), allopurinol, dibenzyline, ATP-MgCl2 and aspartic acid enhance significantly the ischemia-tolerance of liver in vitro.
D000818:Animals; D066298:In Vitro Techniques; D007511:Ischemia / Q000503:physiopathology / Q000517:prevention & control*; D008099:Liver / Q000098:blood supply* / Q000503:physiopathology; D008111:Liver Function Tests; D008297:Male; D010477:Perfusion; D051381:Rats; D013448:Sulfobromophthalein
D013448:Sulfobromophthalein