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室旁核损伤抑制迷走神经传入刺激诱发的胃分泌。

Vagal afferent stimulation-evoked gastric secretion suppressed by paraventricular nucleus lesion.

作者信息

Rogers R C, Hermann G E

出版信息

J Auton Nerv Syst. 1985 Jul;13(3):191-9. doi: 10.1016/0165-1838(85)90011-6.

DOI:10.1016/0165-1838(85)90011-6
PMID:4031362
Abstract

Studies were performed to evaluate the possibility that the paraventricular nucleus (PVN) of the hypothalamus modulates gastric acid secretion by changing the sensitivity of the gastric secretory control mechanism to vagal afferent input. Under pentobarbital anesthesia, 17 rats were prepared with esophageal and pyloric catheters such that the stomach could be perfused continuously on a flow-through basis. Thus, acid secretion could be monitored throughout the experiment. Stimulating electrodes were attached to the central cut end of the cervical vagus nerve. Unilateral stimulation of cervical vagal afferents resulted in a substantial increase in gastric acid secretion. This vagal afferent-mediated increase in acid outflow was suppressed following a single PVN lesion ipsilateral to the side of afferent stimulated output. Given the nature of PVN connections with brainstem regions responsible for the elaboration of vago-vagal reflexes, our results suggest that the PVN may control gastric acid outflow by changing the gain of gastric vago-vagal reflexes.

摘要

开展了多项研究,以评估下丘脑室旁核(PVN)是否通过改变胃分泌控制机制对迷走神经传入输入的敏感性来调节胃酸分泌。在戊巴比妥麻醉下,为17只大鼠植入食管和幽门导管,以便能以连续流通的方式对胃进行灌注。因此,在整个实验过程中都可以监测胃酸分泌。将刺激电极连接到颈迷走神经的中枢切断端。单侧刺激颈迷走神经传入神经会导致胃酸分泌大幅增加。在与受刺激传入输出侧同侧的PVN单次损伤后,这种由迷走神经传入介导的酸流出增加受到抑制。鉴于PVN与负责迷走-迷走反射形成的脑干区域的连接性质,我们的结果表明,PVN可能通过改变胃迷走-迷走反射的增益来控制胃酸流出。

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Vagal afferent stimulation-evoked gastric secretion suppressed by paraventricular nucleus lesion.室旁核损伤抑制迷走神经传入刺激诱发的胃分泌。
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引用本文的文献

1
Brainstem circuits regulating gastric function.调节胃功能的脑干回路。
Annu Rev Physiol. 2006;68:279-305. doi: 10.1146/annurev.physiol.68.040504.094635.
2
Oxytocin excites gastric-related neurones in rat dorsal vagal complex.催产素可兴奋大鼠迷走神经背侧复合体中与胃相关的神经元。
J Physiol. 1990 Sep;428:95-108. doi: 10.1113/jphysiol.1990.sp018202.