Microembolization induced oxygen utilization impairment in the canine gracilis muscle.

Impaired peripheral oxygen utilization coinciding with an elevated cardiac index, venous oxygen tension, and serum lactate with the loss of reactive hyperemic response have been observed in a large series of resuscitated trauma patients. We tested the hypothesis that these clinical findings were due to an alteration of the microcirculation caused by embolization of intravascular particulate matter. To test this hypothesis, we used the bilateral pump-perfused, isolated canine gracilis muscle preparation which we subjected to microembolization with 15 micrometers polystyrene spheres. Prior to microembolization, oxygen consumption was flow-limited up to 6 ml min-1 (r = .928) and at higher flows, oxygen consumption was independent of flow. Following microembolization, the relationship of oxygen consumption and blood flow remained correlated (r = .893), but there was less oxygen consumption at any given flow rate (P less than .05). Imidazole, 30 mg kg-1, IP administered to prevent platelet aggregation, resulted in the return of oxygen utilization to the preembolization value. PVO2 of the microembolized muscle was significantly higher than in the contralateral muscle, which was abolished after imidazole administration. These data suggest that microembolization leads to an oxygen utilization defect similar to that observed in the resuscitated trauma patient. Since this defect was reversed by imidazole administration, a humoral mechanism in the microcirculatory bed may act to restrict oxygen utilization following microembolization and trauma.