Haglund U, Abe T, Ahrén C, Braide I, Lundgren O
Eur Surg Res. 1976;8(5):435-47. doi: 10.1159/000127888.
Mucosal lesions were produced in feline small intestine by evoking a simulated intestinal shock (local hypotension at 30 mm Hg and stimulation of regional sympathetic vasoconstrictor nerves at 6 Hz for 2 h). The degree of mucosal damage was correlated to the level of intestinal blood flow. Microscopically characteristic lesions developed regularly in the small intestinal mucosa when intestinal blood flow was reduced below 12 ml/min X 100 g during the regional shock. The mucosal damage was graded histologically. No difference was found between untreated controls and cats in which the intestinal lumen was perfused with nitrogenated saline. Perfusion with oxygenated saline and i.v. injections of methylprednisolone on the other hand, prevented almost completely the development of the lesions. Albumin, activated charcoal and aprotinin instilled into the intestinal lumen reduced to some extent the mucosal damage. The obtained data support the view that hypoxia is the key factor in the pathogenesis of the mucosal lesions. However, epithelial and intraluminal enzymes are probably important contributing factors.
通过引发模拟肠休克（局部低血压至30毫米汞柱，并以6赫兹频率刺激局部交感缩血管神经2小时）在猫小肠中产生黏膜损伤。黏膜损伤程度与肠血流量水平相关。当局部休克期间肠血流量降至低于12毫升/分钟×100克时，小肠黏膜会规律性地出现显微镜下特征性损伤。对黏膜损伤进行组织学分级。未处理的对照组与肠腔用充氮盐水灌注的猫之间未发现差异。另一方面，用充氧盐水灌注和静脉注射甲基泼尼松龙几乎完全阻止了损伤的发展。向肠腔内注入白蛋白、活性炭和抑肽酶在一定程度上减轻了黏膜损伤。所获得的数据支持以下观点，即缺氧是黏膜损伤发病机制中的关键因素。然而，上皮和腔内酶可能是重要的促成因素。
