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猫后肢肌肉等长收缩期间中脑导水管周围灰质中免疫反应性β-内啡肽释放的抑制作用:可乐定的影响。

Inhibition in the release of immunoreactive beta-endorphin from the periaqueductal grey during isometric contractions of cat hind-limb muscles: the effects of clonidine.

作者信息

Williams C A, Holtsclaw L I, Nichols L P, Brien P L, Chiverton J A

机构信息

Department of Physiology, College of Medicine, East Tennessee State University, Johnson City 37614-0576.

出版信息

Neuropeptides. 1994 Jan;26(1):11-9. doi: 10.1016/0143-4179(94)90087-6.

DOI:10.1016/0143-4179(94)90087-6
PMID:8159281
Abstract

Glass microelectrodes, coated with antibodies specific for beta-endorphin, were inserted into the right periaqueductal grey (PAG) (at PO.5-1.0 mm, LR 2.0 mm and 6.0 mm below the dorsal surface of the colliculi) of cats anesthetized with alpha-chloralose to determine whether immunoreactive beta-endorphins (ir-END) were released in response to fatiguing isometric contractions of the hind-limb muscles. Probes were inserted into the PAG prior to, during and following muscle contraction in the absence or presence of clonidine. ir-END was released from the PAG up to 3 h after surgery was completed while cats remained at rest. In the absence of clonidine, mean arterial pressure increased by 65 +/- 12 mmHg during contractions and the release of ir-END was inhibited during the contraction periods compared to resting periods. Clonidine abolished the pressor response to muscular contraction when injected into the PAG, but did not cause the release of ir-END during fatiguing isometric contractions. These data suggest that isometric contractions of skeletal muscle do not induce the release of ir-END-like substances from the PAG and clonidine does not attenuate the muscle pressor response by causing the release of ir-END from this level in the PAG.

摘要

将涂有针对β-内啡肽的特异性抗体的玻璃微电极插入用α-氯醛糖麻醉的猫的右侧导水管周围灰质(PAG)(位于丘脑海平面以下PO.5 - 1.0 mm、LR 2.0 mm和6.0 mm处),以确定免疫反应性β-内啡肽(ir-END)是否会因后肢肌肉疲劳性等长收缩而释放。在肌肉收缩前、收缩期间和收缩后,在不存在或存在可乐定的情况下,将探针插入PAG。在手术完成后长达3小时内,当猫处于休息状态时,ir-END从PAG中释放出来。在不存在可乐定的情况下,收缩期间平均动脉压升高65±12 mmHg,与休息期相比,收缩期ir-END的释放受到抑制。当将可乐定注入PAG时,它消除了对肌肉收缩的升压反应,但在疲劳性等长收缩期间并未引起ir-END的释放。这些数据表明,骨骼肌的等长收缩不会诱导PAG释放ir-END样物质,并且可乐定不会通过引起PAG此水平的ir-END释放来减弱肌肉升压反应。

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