Abstract

On the basis of previous studies in our laboratory we postulated that the ethanol-induced alteration in jejunal morphology was the result of its effect on the microcirculation. The present study was undertaken to examine the validity of this hypothesis. Accordingly, the effects of intraluminal ethanol perfusion (3.0 and 6.0% w/v) on mucosal morphology; water, glucose, and sodium transport; and regional blood flow were examined in in vivo jejunal segments of pentobarbital-anesthetized dogs. Compared to control segments, those perfused with ethanol exhibited a significant increase in the prevalence of morphological alterations of the mucosa, consisting of subepithelial fluid accumulation (bleb formation) and exfoliation. Those villi with epithelial damage exhibited villus cores significantly shorter than those with a normal, undamaged epithelium. Segments perfused with ethanol exhibited a depressed net water absorption, to the point that net secretion occurred in the segments perfused with 6% ethanol. Net absorption of glucose was similarly depressed by intraluminal perfusion with ethanol, whereas net absorption of sodium was unaffected. Regional jejunal blood flows were estimated using a dual, radiolabeled microsphere technique. Both total jejunal wall and total mucosal blood flow (in ml/min/100 g dry tissue) in the ethanol-perfused segments were significantly increased over control. Similarly, jejunal wall and mucosal capillary blood flows were increased by ethanol perfusion. Neither submucosal nor muscularis blood flows were affected by intraluminal perfusion with ethanol. Compared to control, shunting or nonentrapment of 9-micron microspheres was increased in the mucosa of the ethanol-perfused segments. In contrast to this, shunting of 9-micron microspheres in the submucosa and muscularis was unaffected by intraluminal perfusion with ethanol. It therefore appears that the ethanol-induced mucosal morphological alterations are accompanied by a localized mucosal hyperemia, and an increased shunting of blood through the mucosa. Based on the results of this and other studies, a microvascular mechanism was tentatively proposed to explain the pathogenesis of the ethanol-induced morphological changes.

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