Beck I T, Morris G P, Buell M G
Gastroenterology. 1986 May;90(5 Pt 1):1137-45. doi: 10.1016/0016-5085(86)90378-1.
We have demonstrated previously that ethanol causes alterations in jejunal morphology and fluid secretion, and that these changes are accompanied by an increase in mucosal arteriolar blood flow, shunting of blood through noncapillary microvessels, hyperemia, hemoconcentration, and an enhanced loss of plasma protein into the gut lumen. All the microcirculatory changes are compatible with an ethanol-induced mucosal microvascular stasis. The present study was undertaken to examine whether these changes are accompanied by an enhanced mucosal microvascular permeability. Using a colloidal carbon vascular labeling technique, we demonstrated that 6% wt/vol intraluminal ethanol caused marked accumulation of carbon particles in the walls of the capillaries and microvenules of the villus tips. The effect of 3% ethanol was much less pronounced, and the extent of carbon entrapment did not significantly differ from microvessels in villi perfused with Krebs-Ringer solution without ethanol. Electron microscopy indicated that the carbon was localized between the endothelial cell and the basal lamina of the microvessels. Because the carbon accumulation was always localized at the vicinity of endothelial cell junctions, the escape of carbon particles from the lumen probably occurred through these cell junctions. This could have been the result of a transient retraction of endothelial cells. Electron microscopic examination also demonstrated that the lumina of some capillaries and venules of the villus tip of jejunal segments perfused with 6% ethanol were clogged with carbon particles. This latter finding indicates that there was stasis in these vessels at the time of carbon injection. Similar intraluminal carbon accumulation was never seen in control jejunum or jejunum perfused with 3% ethanol. Thus the results of this study indicate that 6% (wt/vol) ethanol causes microvascular injury and stasis. The findings with 6% ethanol are reminiscent of those described by others in the early phases of acute inflammation, and thus it is possible that the microvascular changes caused by ethanol may be related to the liberation of some of the chemical mediators of the immediate response to acute injury.
我们之前已经证明，乙醇会导致空肠形态和液体分泌发生改变，并且这些变化伴随着黏膜小动脉血流量增加、血液通过非毛细血管微血管分流、充血、血液浓缩以及血浆蛋白向肠腔内的丢失增加。所有这些微循环变化都与乙醇诱导的黏膜微血管淤滞相符。本研究旨在检验这些变化是否伴随着黏膜微血管通透性增强。使用胶体碳血管标记技术，我们证明6%（重量/体积）的腔内乙醇会导致绒毛尖端毛细血管和微静脉壁中碳颗粒的明显积聚。3%乙醇的作用则不太明显，并且碳截留程度与用不含乙醇的 Krebs-Ringer 溶液灌注的绒毛中的微血管没有显著差异。电子显微镜检查表明，碳位于微血管的内皮细胞和基膜之间。由于碳的积聚总是局限在内皮细胞连接处附近，碳颗粒从管腔中逸出可能是通过这些细胞连接发生的。这可能是内皮细胞短暂回缩的结果。电子显微镜检查还表明，用6%乙醇灌注的空肠段绒毛尖端的一些毛细血管和小静脉管腔被碳颗粒堵塞。后一发现表明在注入碳时这些血管存在淤滞。在对照空肠或用3%乙醇灌注的空肠中从未见过类似的腔内碳积聚。因此，本研究结果表明6%（重量/体积）的乙醇会导致微血管损伤和淤滞。6%乙醇的这些发现让人想起其他人在急性炎症早期阶段所描述的情况，因此乙醇引起的微血管变化可能与急性损伤即时反应的一些化学介质的释放有关。
