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[中脑导水管周围灰质在兔体神经对心脏缺血中央抑制中的作用及其机制]

[The role of midbrain periaqueductal grey in the inhibition of central cardiac ischemia by somatic nerve and its mechanism in rabbits].

作者信息

Zhang X, Zhang R

机构信息

Department of Physiology, Zhejiang Medical University.

出版信息

Zhen Ci Yan Jiu. 1991;16(1):5-9.

PMID:1873902
Abstract

UNLABELLED

Experiments were performed on vagotomized male rabbits weighing 1.8-2.2 kg. Urethane and chloralose were administered intravenously, and were paralyzed by flaxedil. After a cannula was inserted into femoral artery to measure blood pressure, the epicardial electrogram (EECG) was recorded. Then we inserted a bipolar electrode into caudal dorsolateral subdivision of periaqueductal grey (CDL), or dorsomedial hypothalamic nucleus (DMH). In some animals, a microinjecting tube was inserted into CDL for microinjection of enkephalin antibodies. In 12 animals, stimulation of CDL could elicit pressor response and elevation of EECG-ST segment. When stimulating deep peroneal nerve, these two responses were inhibited. In 14 animals, with brainstem transected in P5 level, the stimulation of DPN could not inhibit the presser response induced by CDL, but still inhibited the EECG-ST segment changes. After enkephalin antibodies were injected into CDL, DPN could not inhibited EECG-ST changes. In 4 animals, instead of enkephalin antibodies, rabbit serum had no effects. The unit discharges of 96 neurons in CDL were recorded by glass microelectrodes, among them, 15 neurons could be excited by DMH stimulation. We called these neurons the defence reaction related neurons. Stimulation of DPN or median nerve could inhibit the spontaneous discharge and DMH evoked discharge of these defence reaction related neurons.

CONCLUSIONS

  1. DPN stimulation can inhibit the pressor response and cardiac ischemia induced by defence reaction centre in CDL of PAG. The inhibitory effect on cardiac ischemia is still eminently remained after the brainstem is cut in P5 level to eliminate the influence of hypothalamic arcuate nucleus.(ABSTRACT TRUNCATED AT 250 WORDS)
摘要

未标记

对体重1.8 - 2.2千克的雄性迷走神经切断兔进行实验。静脉注射乌拉坦和氯醛糖,并用三碘季铵酚使其麻痹。在股动脉插入插管测量血压后,记录心外膜心电图(EECG)。然后将双极电极插入导水管周围灰质尾背外侧亚区(CDL)或下丘脑背内侧核(DMH)。在一些动物中,将微量注射管插入CDL用于注射脑啡肽抗体。在12只动物中,刺激CDL可引发升压反应和EECG - ST段抬高。刺激腓深神经时,这两种反应均被抑制。在14只动物中,在P5水平横断脑干后,刺激DPN不能抑制CDL诱导的升压反应,但仍能抑制EECG - ST段变化。向CDL注射脑啡肽抗体后,DPN不能抑制EECG - ST段变化。在4只动物中,注射兔血清而非脑啡肽抗体则无作用。用玻璃微电极记录了CDL中96个神经元的单位放电,其中15个神经元可被DMH刺激兴奋。我们将这些神经元称为防御反应相关神经元。刺激DPN或正中神经可抑制这些防御反应相关神经元的自发放电和DMH诱发的放电。

结论

  1. 刺激DPN可抑制PAG的CDL中防御反应中枢诱导的升压反应和心脏缺血。在P5水平切断脑干以消除下丘脑弓状核的影响后,对心脏缺血的抑制作用仍然显著存在。(摘要截断于250字)

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