- Klemcke, Harold G; Ryan, Kathy L; Britton, Steven L; Koch, Lauren G; Dubick, Mich A; Convertino, Victor A
- Hemorrhagic shock reflects low tissue perfusion that is inadequate to maintain normal metabolic functions. Often associated with this condition are impairments in cellular oxygen delivery and utilization. Rat strains divergent in their running endurance have been artificially selected over 12 generations. As these rats bred for high (HCR) vs low (LCR) aerobic running capacity have greater tissue O(2) utilization capacity and improved cardiovascular function, we hypothesized that HCR would be more tolerant (i.e., have greater survivability) to the global ischemia of hemorrhagic shock than LCR. To address this hypothesis, survival time to a severe-as substantiated by dramatic changes in plasma lactate, HCO(3), and base deficit-controlled hemorrhage was measured. Male rats were catheterized and, approximately 24 h later, an estimated >35% of the calculated blood volume was removed during a 26-min period while the rats were conscious and unrestrained. Rats were observed for 6 h or until death. Contrary to our hypothesis, survival time in HCR (220 +/- 63 min; n = 6) did not differ statistically (P = 0.46) from that in LCR (279 +/- 53 min; n = 7). Similarly, there were no statistical differences (P >or= 0.08) between rat lines in blood pH, lactate, HCO(3), and base deficit pre- or post-hemorrhage. In addition, few significant differences between lines in response to hemorrhage were detected by measures of cellular antioxidant status in heart, liver, or lung. Since animals with genetically greater tissue oxygen utilization capacity failed to show longer survival times, our results suggest that other mechanisms must play a more dominant role in determining survivability to hemorrhage under conditions of this hemorrhage.
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