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Microembolization induced oxygen utilization impairment in the canine gracilis muscle
Advances in Shock Research
|January 1, 1981
Summary
Microembolization impairs oxygen use in tissues, similar to trauma patients. This defect was reversed by imidazole, suggesting a humoral mechanism restricts oxygen utilization after trauma and embolization.
Area of Science:
- Physiology
- Microcirculation Research
- Trauma Medicine
Background:
- Resuscitated trauma patients often exhibit impaired peripheral oxygen utilization despite adequate cardiac output.
- Elevated venous oxygen tension and lactate levels suggest a problem with oxygen delivery or utilization at the tissue level.
- The loss of reactive hyperemia in these patients indicates potential microcirculatory dysfunction.
Purpose of the Study:
- To investigate the hypothesis that microcirculatory alterations due to intravascular particulate matter embolization cause impaired oxygen utilization observed in trauma patients.
- To determine if microembolization in a controlled setting replicates the observed physiological derangements in trauma patients.
- To explore potential therapeutic interventions targeting microcirculatory dysfunction.
Main Methods:
- Utilized a bilateral pump-perfused, isolated canine gracilis muscle preparation.
- Induced microembolization using 15-micrometer polystyrene spheres.
- Measured oxygen consumption and venous oxygen tension (PVO2) in relation to blood flow before and after microembolization.
- Administered imidazole to assess its effect on oxygen utilization and PVO2, specifically to inhibit platelet aggregation.
Main Results:
- Microembolization significantly reduced oxygen consumption at any given blood flow rate compared to pre-embolization levels (P < .05).
- Following microembolization, PVO2 was significantly higher in the affected muscle.
- Imidazole administration restored oxygen utilization to pre-embolization levels and abolished the elevated PVO2, indicating reversal of the defect.
Conclusions:
- Microembolization of the microcirculation leads to an oxygen utilization defect mirroring that seen in resuscitated trauma patients.
- The findings suggest that a humoral mechanism within the microcirculatory bed may restrict oxygen utilization following microembolization and trauma.
- Imidazole's efficacy suggests that platelet aggregation and associated humoral factors play a role in this post-trauma/embolization circulatory derangement.