Modification of hyperbaric oxygen toxicity by experimental venous admixture.

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Abstract
The development of oxygen poisoning was compared in 10 normal dogs and in 10 with large veno-arterial shunts produced by anastomosis of the inferior vena cava to the right inferior pulmonary vein 2 weeks before exposure to O2. The control dogs breathed O2 in a hyperbaric chamber at 2.5 atm abs until convulsions (5.1 [plus or minus] SD 2.12 hr) and at 2 atm until death (total 12.3 [plus or minus] 1.4 hr). The operated dogs were exposed to 2.5 atm abs for 5.1 hr and to 2.0 atm abs until death. They experienced no convulsions and survived 21.1 [plus or minus] 2.3 (P < 0.001). The lungs of both groups showed severe damage characteristic of pulmonary O2 toxicity. Minimal lung changes were found in 7 of 8 operated dogs exposed on the same schedule but sacrificed at the median survival time of control dogs. Venous admixture largely prevented elevation of arterial PO2 in the operated dogs during O2 exposure. Delayed development of lung damage and near doubling of survival time are consistent with the hypothesis that pulmonary O2 toxicity is not governed by alveolar oxygen pressure alone but involves factors related to arterial PO2.