Ethanol-induced mucosal microvascular stasis and enhanced plasma protein loss in the dog jejunum

On the basis of previous studies in our laboratory, we have proposed that ethanol-induced alterations in the mucosal microcirculation, particularly vascular stasis, may be responsible for the genesis of the mucosal morphologic lesions and enhanced fluid secretion observed during acute perfusion of the jejunum with ethanol. In an attempt to substantiate this in the present study, we examined (a) the effects of acute intraluminal alcohol perfusion (3.0% and 6.0% wt/vol) on canine mucosal arteriolar blood flow, mucosal red blood cell volume, and mucosal "plasma volume" (as reflected by total mucosal albumin volume), and (b) whether ethanol induces an enhanced secretory filtration of plasma from the jejunal mucosal microvasculature into the gut lumen. These studies indicate that intraluminal perfusion of the jejunum with 6% ethanol leads to a significant (p less than 0.05) increase in both mucosal arteriolar blood flow and red blood cell volume. Despite these changes, mucosal "plasma volume" (total albumin volume) remained unaltered, indicating that hemoconcentration had occurred in the mucosa of the ethanol-perfused segments. These events could result in congestion or stasis within the blood vessels of the mucosa. Perfusion with 6% ethanol also caused a significant increase (p less than 0.05) in the loss of plasma proteins from the mucosal microvasculature into the gut lumen. These results are consistent with our previous proposal that ethanol leads to mucosal microvascular stasis and plasma transudation and that these conditions may in turn lead to the mucosal morphologic lesions and altered fluid transport induced by ethanol.