吗啡和纳洛酮对损毁下丘脑诱致的大鼠胃粘膜损伤之影响

本实验观察了静注吗啡和纳洛酮对电解损毁后部下丘脑诱致的大鼠胃粘膜损伤的影响并观察了在静注吗啡、纳洛酮后和侧脑室注射纳洛酮后其胃酸分泌和血清胃泌素水平之变化。实验揭示,吗啡仅略为降低该神经源性胃粘膜损伤程度,而纳洛酮则明显地减少其胃粘膜损伤;静注吗啡能抑制后部下丘脑损毁后大鼠的胃酸分泌,增加其血清胃泌素水平,而静注纳络酮后,这种大鼠的胃酸分泌增加,但血清胃泌素水平无明显变化;侧脑室注射纳洛酮对后部下丘脑损毁后大鼠胃酸分泌和血清胃泌素水平无明显影响。本结果表明,胃酸可能是导致这种消化道损伤的条件之一,而不是最重要因素;静注纳洛酮对后部下丘脑损毀后大鼠胃粘膜变化有保护作用。后者提示,内源性阿片样肽可能参与这种神经源性胃粘膜损伤的形成。

EFFECTS OF MORPHINE AND NALOXONE ON GASTRIC MUCOSAL INJURY INDUCED BY LESION OF HYPOTHALAMUS IN RATS

The experiment was performed in 90 rats anesthetized with urethene (100mg/100g,intraperitoneally) .In present study we observed the effects of intravenous administration of morphine and naloxone on the gastric mucosal injury induced by electrolytic lesion of the posterior hypothalamus. We also observed the effects of intravenous injection of morphine and naloxone and of injection of naloxone into the lateral cerebral ventricles on the gastric acid secretion and serum gastrin level in rats bearing the lesion in the pos-terior hypothalamus. The results were as followss1. Morphine produced a slight reduction and naloxone did a significant reduction in the gastric mucosal injury compared to control animal when in-travenously administrated.2. The intravenous administration of morphine inhibited gastric acid secretion and enhanced serum gastrin level, but naloxone given by the same route produced an increase in the gastric acid secretion and no significant effect oh the serum gastrin level in the rats with the lesion of the posterior hyptothalamas.3.The gastric acid secretion and serum gastrin level showed no significant changes following the intracerebroventricular administration of nalo-xone in the rats with the lesion of the posterior hypothalamus.The data presented indicated that the presence of gastric acid is probably one of the prerequisites for the development of such a gastric mucosal injury, but not the most important pathogenetic factor in its development. The cytoprotective effect of naloxone on the gastric mucous membrane suggested that the endogenous opiod peptides probably participated in the formation of neurogenetically induced gastric mucosal injury.