Shock : molecular, cellular, and systemic pathobiological aspects and therapeutic approaches : the official journal the Shock Society, the European Shock Society, the Brazilian Shock Society, the International Federation of Shock Societies
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We postulated that hypertonic solutions could minimize the accumulation of lung water and subsequent respiratory derangements that occur after pulmonary contusion. Anesthetized pigs underwent contusion of the right chest at baseline and then were hemorrhaged (30 cc/kg) over 20 min. They were resuscitated with either 7.5% NaCl (4 cc/kg) or .9% saline (90 cc/kg) for 20 min and observed for 4 h. ⋯ Static compliance measurements were significantly decreased from baseline in both groups following pulmonary contusion. There were no differences in wet to dry lung weights or computed tomography scan injury volume between groups. We conclude that small volume hypertonic saline resuscitation does not reduce the magnitude of lung injury or provide substantial physiologic benefit over isotonic solutions following pulmonary contusion.
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To determine the contribution of xanthine oxidase-mediated reperfusion injury to the blood flow deficits seen in the intestinal microcirculation after resuscitated hemorrhagic shock, rats were prepared for intravital microscopic study then bled to 50% of baseline blood pressure for 60 min. Treatment animals received a 50 mg/kg bolus and a 25 mg/kg/h infusion of the xanthine oxidase inhibitor allopurinol after shock but before standard resuscitation with shed blood and an equal volume of Ringer's lactate. A similarly resuscitated group served as control. ⋯ Blood flow in first order arterioles 120 min postresuscitation was 41% of baseline in the standard resuscitation group and 77% of baseline in the allopurinol-treated group. A1 arteriolar diameter was not significantly different between the two groups, being 73 and 82% of baseline, respectively. These data suggest that xanthine oxidase-mediated ischemia-reperfusion injury contributes to blood flow deficits in the small intestinal microcirculation after resuscitated hemorrhagic shock and that the improvement in blood flow seen with allopurinol is not due to vasodilation within the microvasculature.