LUNG INJURY FROM GUT ISCHEMIA

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Abstract
Gut ischemia/reperfusion (I/R) appears to produce pulmonary vascular injury through endotoxin release and cytokine activation. The ability of hepatic reticuloendothelial cells to clear bacterial products may also be impaired during I/R. To test this, diversion of the splanchnic blood flow from the liver into the systemic circulation was performed via a microsurgical portacaval transposition in anesthetized Sprague-Dawley rats (275–375 g). Shunted animals underwent portacaval transposition and were allowed to recover for 7–10 days; sham animals underwent exploration but no shunt was created. The I/R animals were subjected to 60 minutes of reperfusion. All shunts were patent at autopsy. Pulmonary vascular permeability was assessed by measuring tissue retention of Evans blue dye. Gut I/R produced significant increases in pulmonary vascular permeability (46.2% ± 11.0% vs. 16.4% ± 3.8% [I/R vs. control]; p < 0.05) regardless of the presence of hepatic bypass (32.7% ± 9.0% vs. 10.0% ± 1.4% [I/R vs. control]; p < 0.05). These data indicate that a mediator or mediators of gut origin are responsible for pulmonary vascular permeability changes following gut I/R and are not appreciably modulated by the liver.

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