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德尔塔阿片受体参与在麻醉大鼠中二肽啡的心肺作用。

Delta opioid receptors contribute to the cardiorespiratory effects of biphalin in anesthetized rats.

机构信息

Laboratory of Respiratory Reflexes, Mossakowski Medical Research Centre, Polish Academy of Sciences, Pawińskiego 5, PL 02-106 Warszawa, Poland.

出版信息

Pharmacol Rep. 2011;63(5):1235-42. doi: 10.1016/s1734-1140(11)70644-2.

Abstract

Biphalin expresses almost equal affinity for μ- and δ-opioid receptors. The aim of this study was to delineate a possible role of δ-opioid receptors in the cardio-respiratory effects of systemic injection of biphalin in anesthetized, spontaneously breathing rats. In control animals, an intravenous bolus of biphalin (0.3 μmol/kg) evoked apnea, followed by a decreased breathing rate and increased tidal volume, hypotension and bradycardia. Blockade of δ-opioid receptors with naltrindole (4.2 μmol/kg) significantly reduced the duration of apnea, slowdown of respiration, immediate post-challenge hypotension and bradycardia induced by biphalin administration. These results indicate that the activation of δ-opioid receptors adds to the depressive response produced by biphalin.

摘要

脑啡肽表达出对μ-和δ-阿片受体几乎相等的亲和力。本研究旨在描述 δ-阿片受体在全身注射脑啡肽对麻醉、自主呼吸大鼠心肺作用中的可能作用。在对照动物中,静脉内推注脑啡肽(0.3 μmol/kg)可引起呼吸暂停,随后呼吸频率减慢,潮气量增加,低血压和心动过缓。用纳曲吲哚(4.2 μmol/kg)阻断 δ-阿片受体可显著减少脑啡肽引起的呼吸暂停持续时间、呼吸减慢、即刻后挑战性低血压和心动过缓。这些结果表明,δ-阿片受体的激活增加了脑啡肽产生的抑制反应。

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