Resuscitation from hemorrhagic shock causes hepatic injury that is sim
ilar to the hypoxic injury caused by reperfusion after ischemia. This
study was designed to describe the relationship between severe hemorrh
agic shock, hepatic injury, and lipid peroxidation. Fasted Sprague-Daw
ley rats underwent shock (mean arterial pressure 40 +/- 5 mm Hg) for t
wo hours followed by reinfusion of shed blood. Serum ALT levels increa
sed during shock and gradually continued to increase for 24 hours afte
r resuscitation. Lipid peroxidation was assessed by quantification of
exhaled ethane and by liver content of thiobarbituric acid reactive su
bstances (TBARS). Expired ethane was increased both during shock and a
fter resuscitation. Hepatic content of TBARS remained at baseline leve
ls during shock, but increased after resuscitation. The results sugges
t that severe, non-fatal hemorrhagic shock and resuscitation produces
a modest hepatic injury that is accompanied by lipid peroxidation in t
he liver.