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迷走神经阿片受体参与吗啡对麻醉大鼠呼吸作用的机制研究

Involvement of vagal opioid receptors in respiratory effects of morphine in anaesthetized rats.

作者信息

Kaczyńska K, Szereda-Przestaszewska M

机构信息

Laboratory of Respiratory Reflexes, Polish Academy of Sciences Medical Research Centre, 5 Pawińskiego str., 02-106 Warsaw, Poland.

出版信息

J Physiol Pharmacol. 2005 Jun;56(2):195-203.

PMID:15985702
Abstract

Respiratory effects of morphine injection to the femoral vein were investigated in urethane and chloralose anaesthetized and spontaneously breathing rats, prior to and after midcervical vagotomy. Bolus injection of morphine HCl at a dose of 2 mg/kg of body weight induced depression of ventilation in all rats, due to the significant decrease in tidal volume and to the decline in respiratory rate both pre- and post-vagotomy. Expiratory apnoea of mean duration of 10.0+/-3.4 s was present in the vagally intact rats only. Bilateral midcervical section of the vagus nerve precluded the occurrence of apnoea. Prolongation of the expiratory time (T(E morphine) / T(E control)), which amounted to 10.7+/-2.2-fold in the intact state, was apparently reduced to 1.5+/-0.3-fold after division of the vagi. Morphine significantly decreased mean arterial pressure (MAP) at 30 s after the challenge, the effect persisted for not less than 1 minute and was absent in vagotomized rats. The respiratory changes evoked by morphine reverted to the control level after intravenous injection of naloxone at a dose of 1 mg/kg. Results of this study indicate that opioid receptors on vagal afferents are responsible for the occurrence of apnoea and hypotension evoked by morphine.

摘要

在颈中部迷走神经切断术前和术后,对用乌拉坦和氯醛糖麻醉并自主呼吸的大鼠经股静脉注射吗啡的呼吸效应进行了研究。以2mg/kg体重的剂量推注盐酸吗啡,导致所有大鼠通气抑制,这是由于潮气量显著减少以及迷走神经切断术前和术后呼吸频率均下降所致。仅在迷走神经完整的大鼠中出现平均持续时间为10.0±3.4秒的呼气性呼吸暂停。双侧颈中部切断迷走神经可防止呼吸暂停的发生。呼气时间延长(T(E吗啡)/T(E对照)),在完整状态下为10.7±2.2倍,在切断迷走神经后明显降至1.5±0.3倍。吗啡在激发后30秒显著降低平均动脉压(MAP),这种效应持续不少于1分钟,而在迷走神经切断的大鼠中不存在。静脉注射1mg/kg剂量的纳洛酮后,吗啡引起的呼吸变化恢复到对照水平。本研究结果表明,迷走神经传入纤维上的阿片受体是吗啡引起呼吸暂停和低血压的原因。

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