Rainsford K D
Am J Dig Dis. 1978 Jun;23(6):521-30. doi: 10.1007/BF01072696.
The gastric irritant effects of aspirin were studied in rats treated with a variety of physical and "disease" (inflammatory) stress conditions (which may mimic responses to some stress states encountered clinically) with the object of establishing whether these stress states increase the susceptibility of the gastric mucosa to the potentially ulcerogenic actions of aspirin. While exposure to physical (eg, cold) stress conditions markedly increased the sensitivity of the gastric mucosa to aspirin, exposure to various disease stressors (eg, adjuvant arthritis, acute pain, or paw inflammation) did not appreciably affect the mucosal sensitivity to this drug. Attempts were made to determine the mechanisms of the physical stress plus aspirin interaction by use of pharmacological agents. The results suggest a major involvement of the parasympathetic-vagal, sympathetic, and histamine-producing systems, but not the adrenocortical axis, in this model of gastric ulcerogenesis. No differences were observed in the mucosal uptake of [14C]aspirin, showing that accelerated uptake of the drug is not a factor in the development of gastric ulceration.
在多种身体和“疾病”(炎症性)应激条件(可能模拟临床上遇到的某些应激状态的反应)下处理的大鼠中,研究了阿司匹林的胃刺激性,目的是确定这些应激状态是否会增加胃黏膜对阿司匹林潜在致溃疡作用的易感性。虽然暴露于身体(如寒冷)应激条件下会显著增加胃黏膜对阿司匹林的敏感性,但暴露于各种疾病应激源(如佐剂性关节炎、急性疼痛或爪部炎症)对黏膜对该药物的敏感性没有明显影响。尝试通过使用药理学药物来确定身体应激加阿司匹林相互作用的机制。结果表明,在这个胃溃疡形成模型中,副交感神经 - 迷走神经、交感神经和组胺产生系统起主要作用,而肾上腺皮质轴不起作用。在[14C]阿司匹林的黏膜摄取方面未观察到差异,表明药物摄取加速不是胃溃疡形成的一个因素。