Metabolism and the protection by anesthesia against toxicity of O2 at high pressure

Abstract

Experiments were performed on rats to determine whether the protection which anesthesia (sodium pentobarbital) affords against convulsions in oxygen at high pressure (OHP) of 70–75 psi extends to the pulmonary damage and, if so, whether such protection is due simply to the depression of general metabolism. These experiments showed that anesthesia protected against both the pulmonary damage and the convulsions and that this protection was equally well pronounced whether the metabolic depression was or was not counteracted and elevated by dinitrophenol, L-thyronine, or direct tetanic stimulation of muscle. The results support the conclusion that such protection is not due simply to the depression of general metabolism as has been claimed. They also imply that the potentiation of pulmonary damage in OHP by thyroid and CO2 is not a direct effect but rather is of central origin. The close association between the pulmonary damage and convulsions in OHP justifies the inference that these effects are not separate entities, as has been claimed, and point to the importance of central and neurogenic factors in the causation of this pulmonary damage. hyperbaric oxygenation; oxygen poisoning at high pressure; oxygen convulsion in relation to pulmonary damage; pulmonary edema and congestion in oxygen at high pressure; neurogenic factors and toxicity of oxygen at high pressure; direct and neurogenic effects of oxygen at high pressure on the lungs; pCO2and oxygen poisoning; thyroid and pulmonary damage in oxygen poisoning; protection against oxygen toxicity by pentobarbital, urethan, alpha chloralose, and propylene glycol Submitted on September 11, 1964