Oxygen therapy in hemorrhagic shock

Abstract

Decreased oxygen delivery and cellular hypoxia are important factors in the pathophysiology of hemorrhagic shock. We studied the effects of 100% oxygen at 1 and 3 ATA (atmosphere absolute) in a severe model of hemorrhagic shock induced by bleeding 50% of the total blood volume in rats. Post-treatment with 100% oxygen at 1 and 3 ATA maintained mean arterial blood pressure (MABP) in hemorrhaged rats at significantly higher values compared to untreated controls (P less than 0.01 at 1 and 3 ATA). Treatment with oxygen attenuated the increase in plasma activities of the lysosomal hydrolase cathepsin D (P less than 0.05 at 1 ATA; P less than 0.01 at 3 ATA). Oxygen at 3 ATA also attenuated the plasma accumulation of free amino-nitrogen compounds (P less than 0.05). Furthermore, hyperoxia prevented the final increase in hematocrit (P less than 0.05 at 1 ATA; P less than 0.01 at 3 ATA). Hemorrhaged rats treated with oxygen also exhibited a significantly longer survival time (P less than 0.01 at both doses), and higher survival rates (50% at 1 ATA and 100% at 3 ATA; P less than 0.05 and P less than 0.01, respectively) than untreated shock rats. No significant effect on any of the above mentioned variables was found in hemorrhaged rats treated with 7% oxygen at 3 ATA (oxygen pressure 0.2 ATA), indicating that all salutary effects can be attributed to oxygen and not to the increased ambient pressure per se. Our results indicate that 100% oxygen in normobaric and hyperbaric conditions exerts important beneficial effects in hemorrhagic shock and may be a useful drug for the treatment of this condition.