MESENTERIC VASCULAR RESPONSES TO ENDOTOXIN
OKLAHOMA UNIV MEDICAL CENTER OKLAHOMA CITY
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The hypothesis that septic shock includes mesenteric vasoconstriction as an essential step in the pathogenesis of the disorder was tested. This hypothesis has been based upon experiments using the canine model which does respond to endotoxin by developing mesenteric constriction and ischemia. We measured systemic arterial and portal venous pressures and mesenteric blood flow in 6 anesthetized rhesus monkeys and 6 anesthetized dogs during periods of control and for 4 hours after injection of lethal doses of E. coli endotoxin. Dogs responded as reported previously with abrupt but transient marked portal hypertension, early systemic arterial hypotension and a profound decline in mesenteric blood flow. Calculated vascular resistance steadily increased after endotoxin. In monkeys the circulatory responses were different 1 arterial pressure fell gradually 2 portal pressure increase was small 3 mesenteric blood flow did not decrease and 4 calculated mesenteric vascular resistance decreased steadily following injection of endotoxin. In contrast to previous findings in dogs, it appears that a key step in human septic shock may be mesenteric vasodilation, since the subhuman primate exhibits this hemodynamic response to endotoxin.
- Anatomy and Physiology
- Medicine and Medical Research