Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.6.1.2 (alanine aminotransferase)
 26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An experimental hepatitis was induced in rabbits by intravenous infusion of 1 g galactosamine per kilogram of body weight. Galactosamine administration caused microclot formation in kidneys, liver, lungs, and spleen in a low percentage. If, however, animals were infused with the fibrinolysis inhibitor epsilon-aminocaproic acid in addition to galactosamine, microclots were generated in a high percentage. The microclots exhibited typical staining characteristics like those observed in the generalized Shwartzman reaction. Some animals developed bilateral renal cortical necrosis. Heparin treatment prevented the occurrence of microclot fromation after galactosamine administration, but it neither prolonged the survival time of the animals nor prevented or reduced liver cell damage. Increases in serum GPT and bilirubin levels were similar in heparin-treated and untreated rabbits. The experiments indicate that disseminated intravascular coagulation is involved in galactosamine-induced hepatitis but does not contribute to the severity of the liver injury.
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PMID:Experimental galactosamine-induced hepatitis. Effect of anticoagulant and antifibrinolytic agents on microclot formation. 125 92

A clinicopathological study was undertaken in 15 cases of massive hepatic necrosis after shock. The GOT and GPT level exceeded 1000 units in 10 cases. The 15 cases consisted of 3 diagnosed as fulminant hepatitis clinically and 12 diagnosed as disseminated intravascular coagulation (DIC) or multiple systemic organ failure (MOF) from the unremarkableness of liver dysfunction. It was noteworthy that sepsis and surgery were closely associated with these lesions. The weight of the liver at autopsy ranged from 800 to 2,700 g. Liver necrosis was macroscopically characterized by clear demarcation of the necrotic areas sharply separated from the surrounding liver parenchyma, showing the appearance of so-called "map-like necrosis". Microscopically, the lesions in these subjects showed mainly the pattern of centrilobular necrosis. As observed in the burn shock case (case 12), the shock which provoked in different phases of time seemed to have repeated its attack. These liver necroses were considered to result from severe systemic circulatory disturbance or intrahepatic circulatory disturbance. The possibility is indicated that the generalized or univisceral Shwartzman reaction, and repeated and combined severe shock participated in the pathogenesis. Fibrin thrombi aggrevate tissue perfusion and accelerate anoxia. Heparin therapy seemed effective in these cases if administered at an appropriate time.
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PMID:Fatal hepatic necrosis after shock. 371 91

ELISA was employed to detect changes in plasma TNF-alpha and IL-6 level in rabbits having endotoxin-induced generalized Shwartzman reaction. Liver injury was assessed by the increase of serum ALT and hepatic histopathologic changes. The results showed that plasma TNF-alpha and IL-6 levels increased remarkably 12h after intravenous injection of endotoxin twice at a 24h interval, and these changes corresponded with the degree of liver injury. Coinjection of dexamethasone and endotoxin partly prevented the elevation of TNF-alpha and IL-6 levels and reduced liver injury. These results indicated that TNF-alpha and IL-6 were involved in endotoxin-induced liver injury.
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PMID:Endotoxin-induced liver injury and changes in the levels of plasma tumor necrosis factor-alpha and interleukin-6 in rabbits. 755 77