Pathophysiological Effects of Hemorrhagic Shock and Resuscitation in a Rat Model
Alaimo, Andrew Anthony
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Extensive investigations of the pathophysiology of hepatic no-flow ischemia - reperfusion injury demonstrated substantial Kupffer cell activation with reactive oxygen formation during the first few hours of reperfusion as indicated by increases in plasma glutathione disulfide (GSSG) levels in vivo (Jaeschke et aI., 1991) and enhanced superoxide formation by Kupffer cells (KC) isolated from the postischemic livers (Jaeschke et al.., 1990). To test whether or not similar mechanisms are operative during hepatic ischemia induced by hemorrhagic shock, male Fischer rats (230-250 g) were subjected to 60 min of hemorrhage (mean arterial pressure 40 mm Hg) followed by resuscitation (RS) (reinfusion of shed blood). Hepatic ATP levels declined from 2.3 + 0.2 J.1mol/g to 0.24 + 0.08 (60 min shock) indicating severe ischemia, and recovered to 1.0 + 0.2 at 90 min RS. To test for potential oxidant stress during RS, plasma GSSG concentrations were measured. Although GSSG levels increased by 1200/0 compared to baseline levels (0.69 + 0.31 J.1M), there was no significant difference to that of the animals which experienced hepatic no-flow ischemia. In striking contrast to previous findings with hepatic no-flow ischemia, we found no evidence for a significant KC activation after 60 min of hemorrhagic shock and up to 90 min of resuscitation.