Acute Acalculous Cholecystitis After Trauma: The Role of Microcirculatory Failure and Cellular Hypoxia
AbstractCritical illness is expensive. Neural transmission, ion transport, vasoconstriction, glandular and hormonal secretions are highly endergonic processes that are amplified in the face of trauma, sepsis, or both. It is not surprising, therefore, that the enzymes that drive catabolic reactions (citric acid cycle, oxidative phosphorylation and beta-oxidation), unlike the enzymes of anabolism, are located exclusively in the mitochondrial matrix. Low cardiac output in the aftermath of trauma imposes compensatory responses to divert blood from the rest of the body to the vital organs. Endogenous epinephrine and vasopressin interact synergistically to produce intense splanchnic vasoconstriction and hypoxia. Therapeutic agents (dobutamine, halothane and opioids) have similar adverse effects on the mesenteric microcirculation.
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