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水浸应激下大鼠胃酸分泌及损伤形成

Gastric acid secretion and lesion formation in rats under water-immersion stress.

作者信息

Hayase M, Takeuchi K

出版信息

Dig Dis Sci. 1986 Feb;31(2):166-71. doi: 10.1007/BF01300703.

Abstract

In attempts to investigate the roles of acid in the pathogenesis of stress-induced gastric lesions, gastric acid secretion was studied in pylorus-ligated and lumen-perfused rats under restraint alone (R) or restraint with additional water immersion (WI). Gastric mucosal blood flow (GMBF) was measured with the aminopyrine clearance method in acute fistula rats. Acid secretion in pylorus-ligated rats significantly decreased under R or WI of either 3.5 or 7 hr stress. In the lumen-perfused or acute-fistula rats, exposure of rats to stress for 7 hr produced a similar decrease; however, in the WI group, there was a significant increase of acid secretion for 3-4 hr during stress, but not exceeding the prestress level. Only in the WI group did GMBF exhibit similar increases to those of acid secretory activity, and these increases were significantly inhibited by intraperitoneal administration of atropine (1 mg/kg) or cimetidine (60 mg/kg). Gastric lesions developed in both groups at 3.5 hr and became extensively severe at 7 hr only in the WI group. Cimetidine failed to influence the formation of lesions at 3.5 hr but significantly inhibited the later outgrowth of lesions at 7 hr, while atropine or pylorus ligation all but completely prevented lesions induced by either 3.5- or 7-hr WI stress. These results indicate that exposure of rats to stress (R or WI) generally decreased acid secretory activity, but there was a rise in acid secretion toward normal levels during WI stress, which may play an important role in the aggravating process of stress-induced gastric lesions.

摘要

为了研究胃酸在应激性胃损伤发病机制中的作用,对幽门结扎和管腔灌注的大鼠在单独束缚(R)或束缚加额外水浸(WI)条件下的胃酸分泌进行了研究。采用氨基比林清除法测定急性瘘管大鼠的胃黏膜血流量(GMBF)。在3.5小时或7小时应激的R或WI条件下,幽门结扎大鼠的胃酸分泌显著降低。在管腔灌注或急性瘘管大鼠中,大鼠暴露于应激7小时也产生了类似的降低;然而,在WI组中,应激期间3 - 4小时胃酸分泌显著增加,但未超过应激前水平。只有在WI组中,GMBF表现出与胃酸分泌活性类似的增加,并且这些增加被腹腔注射阿托品(1毫克/千克)或西咪替丁(60毫克/千克)显著抑制。两组在3.5小时时均出现胃损伤,仅WI组在7小时时胃损伤广泛且严重。西咪替丁在3.5小时时未能影响损伤的形成,但在7小时时显著抑制了损伤的后期发展,而阿托品或幽门结扎几乎完全预防了3.5小时或7小时WI应激诱导的损伤。这些结果表明,大鼠暴露于应激(R或WI)通常会降低胃酸分泌活性,但在WI应激期间胃酸分泌会向正常水平升高,这可能在应激性胃损伤的加重过程中起重要作用。

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