Mirkovitch V, Winistörfer B
Res Exp Med (Berl). 1987;187(4):295-302. doi: 10.1007/BF01852055.
The action of dimethyl sulfoxide (DMSO) was investigated employing an experimental model of intestinal perfusion in vivo of isolated loops of dog ileum before, during, and following 1-h ischemia. DMSO was administered either into the intestinal lumen or by a continuous injection via a branch of the artery supplying the experimental loop. In the intact intestine, intraluminal DMSO significantly decreased the net movement of water, electrolytes, and glucose without affecting either the active transport of phenylalanine and beta-methylglucoside or morphology. This inhibition was irreversible since, following DMSO removal, there was only partial recovery of water absorption, while the other parameters remained significantly low. Inhibition by DMSO was delayed when the substance was injected intraarterially (i.a.). Regardless of its route of administration, DMSO did not reduce the extent of ischemic injury in comparison with non-treated "Controls": during ischemia, all functional parameters were practically non-existent. Following the re-establishment of circulation, a net loss of water and electrolytes ensued, and active transport did not improve. In both instances, the structural alterations were those associated with ischemia of the experimental model employed: short, broad, club-shaped villi which had completely lost their epithelium, but fairly intact crypts. It can be concluded from the data presented that in the dog DMSO inhibits absorption in the intact ileum and exerts no protection against ischemic lesion.
采用犬回肠离体肠袢体内灌注实验模型,研究了二甲基亚砜(DMSO)在1小时缺血前、缺血期间及缺血后的作用。DMSO通过肠腔给药,或经供应实验肠袢的动脉分支持续注射给药。在完整肠段中,肠腔内的DMSO显著降低了水、电解质和葡萄糖的净转运,而不影响苯丙氨酸和β-甲基葡萄糖苷的主动转运或形态学。这种抑制是不可逆的,因为去除DMSO后,水吸收仅部分恢复,而其他参数仍显著降低。当DMSO经动脉内注射时,其抑制作用延迟。无论给药途径如何,与未处理的“对照组”相比,DMSO均未降低缺血损伤的程度:在缺血期间,所有功能参数实际上均不存在。循环恢复后,水和电解质出现净丢失,主动转运也未改善。在这两种情况下,结构改变均为所用实验模型缺血相关的改变:短而宽的杵状绒毛,其上皮完全丧失,但隐窝相当完整。从所呈现的数据可以得出结论,在犬中,DMSO抑制完整回肠的吸收,且对缺血性损伤无保护作用。