Restraint stress augments postprandial gastric contractions but impairs antropyloric coordination in conscious rats.
Restraint stress augments postprandial gastric contractions but impairs antropyloric coordination in conscious rats.
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约束压力会增强清醒大鼠的餐后胃收缩，但会损害前幽门协调性。
DOI：
10.1152/ajpregu.00161.2005
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发表时间：
2006
期刊：
影响因子：
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通讯作者：
Takahashi,Toku
中科院分区：
文献类型：
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作者：
Nakade,Yukiomi;Tsuchida,Daisuke;Fukuda,Hiroyuki;Iwa,Masahiro;Pappas,TheodoreN;Takahashi,Toku
中枢促肾上腺皮质激素释放因子（CRF）在抑制应激诱导的胃排空延迟中起重要作用。然而，目前尚不清楚约束应激如何调节胃运动以延缓胃排空。由于胃实体排空是通过幽门协调调节的，我们假设约束应激损害了幽门协调，导致有意识大鼠的胃实体排空延迟。将两个应变计传感器缝合在胃窦和幽门的浆膜表面，并在约束应力之前、期间和之后监测餐后胃运动。幽门协调，定义为在10秒内从胃窦到幽门的扩张性单次收缩，随后是≥20秒的静止。约束应激使餐后胃窦和幽门的胃动力分别提高至基础的140±9%和134±9% （n= 6）。约束应激前的幽门协调发作次数由2.4±0.4/10 min显著减少至0.6±0.3/10 min。腹腔注射CRF 2型受体拮抗剂应激素2B （60 μg）或胍乙啶可部分恢复约束应激诱导的幽门配位损伤（1.6±0.3/10 min,n= 6）。应激素2B和胍乙啶可增强抑制应激引起的心房和幽门收缩，而阿托品、六甲铵和迷走神经切开术可消除抑制应激引起的心房和幽门收缩。约束应激通过迷走神经胆碱能途径增强餐后胃动力。约束应力引起的固体胃排空延迟是由于幽门协调功能的损害。约束应力诱导的幽门协调功能损伤可能通过中央CRF通路介导。
Central corticotropin-releasing factor (CRF) plays an important role in mediating restraint stress-induced delayed gastric emptying. However, it is unclear how restraint stress modulates gastric motility to delay gastric emptying. Inasmuch as solid gastric emptying is regulated via antropyloric coordination, we hypothesized that restraint stress impairs antropyloric coordination, resulting in delayed solid gastric emptying in conscious rats. Two strain gauge transducers were sutured onto the serosal surface of the antrum and pylorus, and postprandial gastric motility was monitored before, during, and after restraint stress. Antropyloric coordination, defined as a propagated single contraction from the antrum to the pylorus within 10 s, was followed by ≥20 s of quiescence. Restraint stress enhanced postprandial gastric motility in the antrum and pylorus to 140 ± 9% and 134 ± 9% of basal, respectively (n= 6). The number of episodes of antropyloric coordination before restraint stress, 2.4 ± 0.4/10 min, was significantly reduced to 0.6 ± 0.3/10 min by restraint stress. Intracisternal injection of the CRF type 2 receptor antagonist astressin 2B (60 μg) or guanethidine partially restored restraint stress-induced impairment of antropyloric coordination (1.6 ± 0.3/10 min,n= 6). The restraint stress-induced augmentation of antral and pyloric contractions was increased by astressin 2B and guanethidine but abolished by atropine, hexamethonium, and vagotomy. Restraint stress enhanced postprandial gastric motility via a vagal cholinergic pathway. Restraint stress-induced delay of solid gastric emptying is due to impairment of antropyloric coordination. Restraint stress-induced impairment of antropyloric coordination might be mediated via a central CRF pathway.