It has been suggested that
septic shock is a disorder of microvascular autoregulation. Tissue blood flow is modulated by the state of activation of upstream endothelial receptors controlling the vascular smooth muscle tone. Because vascular receptor populations vary between organs, it should be expected that vasoactive drugs affect tissue oxygenation differently in different organs. We studied the effects of
dopexamine HCl (a novel inotrope) and
septic shock on
oxygen delivery as well as tissue Po2 in gut, liver, and skeletal muscle in anesthetized rabbits. Employing the thermodilution technique, cardiac output was measured across the pulmonary bed and used to calculate
oxygen delivery. Three eight-channel Mehrdraht Dortmund Oberfläche
oxygen electrodes were placed on gut serosa, liver, and skeletal muscle surfaces, respectively, and sufficient readings were obtained to calculate tissue Po2 distributions. During
septic shock mean arterial pressure, cardiac output,
oxygen delivery, and mean tissue Po2 decreased in all organs. Our results suggest that the observed changes in tissue oxygenation during
septic shock were caused by defective regulation of microvascular blood flow. In conclusion, during baseline conditions
dopexamine HCl caused no statistically significant changes in tissue oxygenation in any organ, except in skeletal muscle
at 10 micrograms/kg/min when tissue Po2 increased. During
septic shock, however,
dopexamine HCl improved oxygenation in all three organs in a dose-dependent manner.