Hauser C J, Locke R R, Kao H W, Patterson J, Zipser R D
Department of Surgery, Hollywood Presbyterian Medical Center, Los Angeles, CA 90027.
J Lab Clin Med. 1988 Jul;112(1):68-71.
The impairment of bowel healing that is characteristic of inflammatory bowel disease (IBD) is poorly understood. Because bowel healing is related to the adequacy of perfusion in other circumstances, we studied bowel surface oxygen tension (PSO2), which is related to bowel perfusion, in rabbits with IBD. Both cell-mediated (n = 17) and immune complex-mediated (n = 10) colitis caused marked attenuation of colon PSO2. Control (n = 13) left colon PSO2 was 36 +/- 5 (SEM) torr. In mild colitis, left colon PSO2 fell to 11 +/- 5 torr, and in severe colitis it fell to 4 +/- 1 torr (p less than 0.01 for each compared with control). These changes occurred irrespective of the mechanism of induction of colitis. Gastric and small intestinal PSO2 were unaffected. Hepatic and renal PSO2 were decreased in severe colitis only. The presence of decreased PSO2 was a better marker for the presence of IBD than was histologic evaluation. It is suggested that attenuation of PSO2 may be a marker for the physiologic activity of IBD. If this is so, PSO2 may prove a useful adjunct in the operative management of IBD.
炎症性肠病（IBD）所特有的肠道愈合受损情况目前了解甚少。由于在其他情况下肠道愈合与灌注充足程度有关，我们研究了患有IBD的兔子的肠表面氧张力（PSO2），其与肠道灌注相关。细胞介导的结肠炎（n = 17）和免疫复合物介导的结肠炎（n = 10）均导致结肠PSO2显著降低。对照组（n = 13）左结肠PSO2为36±5（SEM）托。在轻度结肠炎中，左结肠PSO2降至11±5托，在重度结肠炎中则降至4±1托（与对照组相比，每组p均小于0.01）。这些变化与结肠炎的诱发机制无关。胃和小肠的PSO2未受影响。仅在重度结肠炎中肝脏和肾脏的PSO2降低。PSO2降低比组织学评估更能作为IBD存在的标志物。提示PSO2降低可能是IBD生理活性的一个标志物。如果是这样，PSO2可能在IBD的手术治疗中被证明是一个有用的辅助指标。
