We studied the intraoperative and postoperative effects of anesthesia and wound excision on oxygen delivery and oxygen consumption after burn injury. Twenty adult sheep were studied: six had halothane anesthesia alone and 14 had anesthesia and third-degree burns over 15% of the total body surface. Body temperatures were maintained within 1 degree C of baseline value during the operations. The burns on six sheep were totally excised and hide from donor sheep was grafted 3 hours after injury; in eight sheep, excision and grafting were done 5 days after injury. We found that 3 hours of anesthesia in controls decreased oxygen delivery (DO2) by 22% +/- 6% and oxygen consumption (VO2) by 30% +/- 7% from waking baseline values primarily because of a decrease in cardiac output as oxygen (O2) extraction from hemoglobin also decreased. However, no base deficit developed. DO2 and (VO2) transiently increased to 9% +/- 3% above baseline value on the sheeps' return to the waking state. Anesthesia and wound excision, which began 3 hours after the burns were formed, decreased DO2 and VO2 by 25% +/- 4% and 32% +/- 4%, respectively, despite baseline filling pressures. However, a base deficit of -3 +/- 1 mEq/L developed during the two-hour operations, which began with the administration of anesthesia alone. Oxygen consumption increased to 25% +/- 6% above the waking baseline value upon each subject's return to the waking state. In the sheep treated 5 days after burn injury, DO2 decreased by 35% +/- 6% and VO2 decreased by 42% +/- 6% below the value during the waking hypermetabolic state when the sheep were under anesthesia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

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Increased lipid peroxidation and decreased antioxidant activity correspond with death after smoke exposure in the rat.

Oxidants are released directly from smoke and also as a result of the airways inflammation that occurs after smoke injury. We determined the relation between the degree of tissue oxidant change with the use of malondialdehyde content to measure lipid peroxidation and the degree of lung and systemic organ damage and resulting damage mortality 24 hours after a controlled smoke exposure in a rat model. We also monitored changes in the key tissue antioxidant catalase. We found that the degree of lung lipid peroxidation and the decrease in catalase activity directly correlated with mortality caused by respiratory failure and with the degree of lung inflammation but that they did not correlate with the peak carboxyhemoglobin level, a marker of smoke gas phase exposure. The lung oxidant changes also directly correlated with increased systemic lipid peroxidation and decreased catalase in liver and kidney tissue. We conclude that the initial smoke insult causes lung and in turn systemic inflammation with resulting release of oxidants, which leads to tissue oxidant injury. The degree of lung oxidant change significantly correlates with the degree of lung tissue injury, respiratory failure, and mortality, and the major source of the oxidant changes is tissue inflammation rather than oxidants in the smoke itself.

Animals↗