Hepatic injury and lipid peroxidation during hemorrhagic shock and resuscitation.
Resuscitation from hemorrhagic shock causes hepatic injury that is similar to the hypoxic injury caused by reperfusion after ischemia. This study was designed to describe the relationship between severe hemorrhagic shock, hepatic injury, and lipid peroxidation. Fasted Sprague-Dawley rats underwent shock (mean arterial pressure 40 +/- 5 mm Hg) for two hours followed by reinfusion of shed blood. Serum ALT levels increased during shock and gradually continued to increase for 24 hours after resuscitation. Lipid peroxidation was assessed by quantification of exhaled ethane and by liver content of thiobarbituric acid reactive substances (TBARS). Expired ethane was increased both during shock and after resuscitation. Hepatic content of TBARS remained at baseline levels during shock, but increased after resuscitation. The results suggest that severe, non-fatal hemorrhagic shock and resuscitation produces a modest hepatic injury that is accompanied by lipid peroxidation in the liver.
Dart
R C
RC
Department of Surgery, University of Arizona, Tucson 85724.
Liebler
D C
DC
Sipes
I G
IG
D000818:Animals; D004195:Disease Models, Animal; D004980:Ethane / Q000378:metabolism; D015227:Lipid Peroxidation / Q000502:physiology*; D008099:Liver / Q000378:metabolism; D008107:Liver Diseases / Q000209:etiology* / Q000378:metabolism*; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism; D012151:Resuscitation / Q000009:adverse effects*; D012771:Shock, Hemorrhagic / Q000150:complications* / Q000378:metabolism* / Q000628:therapy; D014811:Vitamin E Deficiency / Q000378:metabolism
D017382:Reactive Oxygen Species; D004980:Ethane