Zeitlin I J, Smith A N
Gut. 1973 Feb;14(2):133-8. doi: 10.1136/gut.14.2.133.
Colonic tissue was taken at operation from 10 patients with active ulcerative colitis and three patients with uncomplicated diverticular disease but with severe symptoms. Levels of kininogen, kallikrein, and kallikrein precursor were measured in blood-free tissue samples. In normal colon tissue a kininogen occurred in the muscle and none was detected in the mucosa. Kallikrein and its precursor were found in mucosa but not in muscle. In acutely inflamed tissue from ulcerative colitis patients relatively high levels of active kallikrein were detected in the underlying colonic muscle. There was little change in the level of kallikrein in inflamed mucosa or of kininogen in the muscle of these patients. No kallikrein was found in colonic muscle from patients with diverticular disease and the mucosal kallikrein level in these patients was unchanged. The findings suggest a mechanism for the formation of kinins in the wall of the colon which is present in ulcerative colitis but not in diverticular disease.
在手术中从10例活动性溃疡性结肠炎患者和3例无并发症但有严重症状的憩室病患者身上获取结肠组织。在无血组织样本中测量激肽原、激肽释放酶和激肽释放酶前体的水平。在正常结肠组织中,激肽原存在于肌肉中,而在黏膜中未检测到。激肽释放酶及其前体在黏膜中发现,但在肌肉中未发现。在溃疡性结肠炎患者的急性炎症组织中,在下层结肠肌肉中检测到相对较高水平的活性激肽释放酶。这些患者炎症黏膜中的激肽释放酶水平或肌肉中的激肽原水平几乎没有变化。憩室病患者的结肠肌肉中未发现激肽释放酶,这些患者的黏膜激肽释放酶水平未改变。这些发现提示了结肠壁中激肽形成的一种机制,这种机制存在于溃疡性结肠炎中,但不存在于憩室病中。