Mechanism of ethanol-induced jejunal microvascular and morphologic changes in the dog.

To study the mechanism of morphologic and microvascular effects of intraluminal ethanol, we perfused jejunal segments of the dog with 6% (wt/vol) ethanol for 0 (control), 10, 20, 30, 60, and 90 min, and measured the time-dependent changes in (a) the prevalence of villi with epithelial damage (i.e., villi with intact blebs plus those with broken blebs) and those without epithelial damage (undamaged villi), (b) the height of the villus core and the patency of lacteals, (c) jejunal albumin loss, and (d) permeability of microvessels of the villus tip by colloidal carbon vascular labeling. We found that (a) the prevalence of villi with epithelial damage or with intact bleb increased progressively during the first 20 min of ethanol perfusion and then declined gradually; (b) the height of the villus core and the patency of lacteals in the undamaged villi and in those with intact bleb decreased during the first 20 min and then gradually increased; and (c) jejunal albumin loss and the prevalence of villi with carbon labeling increased for the first 30 min, after which the former declined gradually whereas the latter remained at a plateau. These findings suggest that contraction of the villus core and compression of the lymphatics are the primary cause of ethanol-induced epithelial damage, which is accentuated by increased microvascular permeability and consequent protein leakage. The mechanism of recovery of most parameters, in spite of continuous ethanol perfusion, remains to be investigated.