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高血糖会损害清醒大鼠的胃窦-幽门协调性并延迟胃排空。

Hyperglycemia impairs antro-pyloric coordination and delays gastric emptying in conscious rats.

作者信息

Ishiguchi Tadashi, Tada Hitoshi, Nakagawa Kazuhiko, Yamamura Takehira, Takahashi Toku

机构信息

Department of Internal Medicine, Wakayama Medical College, Japan.

出版信息

Auton Neurosci. 2002 Jan 10;95(1-2):112-20. doi: 10.1016/s1566-0702(01)00383-6.

Abstract

Delayed gastric emptying has been shown in diabetes. Although it has been proposed that hyperglycemia, and not only autonomic neuropathy, contributes to the pathogenesis of delayed gastric emptying, the inhibitory mechanism of hyperglycemia on gastric emptying remains unclear. We studied the effects of hyperglycemia per se on gastric emptying and postprandial gastric motility in conscious rats. Liquid and solid gastric emptying were compared between saline-infused rats and D-glucose-infused rats. Two strain gauge transducers were implanted on the antrum and pylorus and the postprandial antro-pyloric coordination was compared between euglycemia and hyperglycemia. D-glucose infusion for 30 min increased blood glucose level from 5.4 +/- 0.5 to 13.0 +/- 1.3 mM and significantly delayed gastric emptying. Forty minutes after the feeding, contractions with low frequency (<3 cycles min(-1)) and high amplitude (>15 g) of the antrum were observed. This period reflects the emptying process of the gastric content and the coordination between the antrum and pylorus was frequently observed. D-glucose infusion significantly reduced feeding-induced antral contractions and abolished the number of episodes of antro-pyloric coordination. Sham feeding-induced gastric contractions were also significantly reduced by hyperglycemia. Postprandial antro-pyloric coordination was not observed in vagotomized rats, suggesting a mediation of vagus nerve. It is concluded that hyperglycemia impairs antral contractions and antro-pyloric coordination in rats. The inhibitory effect of hyperglycemia on gastric emptying is mediated, at least in part, via impaired vagal activity.

摘要

糖尿病患者已出现胃排空延迟。尽管有人提出高血糖而非仅自主神经病变是胃排空延迟发病机制的原因,但高血糖对胃排空的抑制机制仍不清楚。我们研究了高血糖本身对清醒大鼠胃排空和餐后胃动力的影响。比较了输注生理盐水的大鼠和输注D-葡萄糖的大鼠的液体和固体胃排空情况。在胃窦和幽门植入两个应变片式传感器,比较了血糖正常和高血糖状态下餐后胃窦-幽门的协调性。输注D-葡萄糖30分钟使血糖水平从5.4±0.5毫摩尔/升升至13.0±1.3毫摩尔/升,并显著延迟胃排空。喂食后40分钟,观察到胃窦出现低频(<3次/分钟)和高幅度(>15克)的收缩。这段时间反映了胃内容物的排空过程,且经常观察到胃窦和幽门之间的协调性。输注D-葡萄糖显著减少了喂食引起的胃窦收缩,并消除了胃窦-幽门协调性的发作次数。假喂食引起的胃收缩也因高血糖而显著减少。在迷走神经切断的大鼠中未观察到餐后胃窦-幽门协调性,提示迷走神经起介导作用。结论是高血糖损害大鼠胃窦收缩和胃窦-幽门协调性。高血糖对胃排空的抑制作用至少部分是通过迷走神经活动受损介导的。

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