L-苯异丙基腺苷（L-PIA）可降低大鼠对氟烷的麻醉需求，并减少去甲肾上腺素能神经传递。

L-phenylisopropyladenosine (L-PIA) diminishes halothane anesthetic requirements and decreases noradrenergic neurotransmission in rats.

作者信息

Birch B D, Louie G L, Vickery R G, Gaba D M, Maze M

机构信息

Department of Anesthesia, Stanford University School of Medicine, Palo Alto, CA.

出版信息

Life Sci. 1988;42(14):1355-60. doi: 10.1016/0024-3205(88)90164-6.

DOI:10.1016/0024-3205(88)90164-6

PMID:2832674

Abstract

The effect of L-phenylisopropyladenosine (L-PIA), the A1 adenosine agonist, on the depth of anesthesia was investigated in halothane-anesthetized rats. L-PIA treatment reduced the minimum anesthetic concentration (MAC) of halothane that prevented 50% of animals from moving in response to a painful stimulus by 49%. MAC experiments performed with L-PIA given in conjunction with A1 adenosine receptor antagonists which either permeate the blood-brain barrier (8-phenyltheophylline [8-PT] or do not (8-sulphophenyltheophylline [8-So-PT]) indicate that central mechanisms are involved. Noradrenergic neurotransmission was diminished following L-PIA administration in halothane-anesthetized rats in all brain regions. These data suggest that acute L-PIA treatment decreases central noradrenergic neurotransmission and may represent the mechanism for the decrease in halothane dose to achieve an anesthetic endpoint anesthetic response to halothane.

摘要

在氟烷麻醉的大鼠中研究了A1腺苷激动剂L-苯异丙基腺苷（L-PIA）对麻醉深度的影响。L-PIA处理使氟烷的最小麻醉浓度（MAC）降低了49%，该浓度可防止50%的动物对疼痛刺激产生移动反应。与可穿透血脑屏障的A1腺苷受体拮抗剂（8-苯基茶碱[8-PT]）或不可穿透血脑屏障的A1腺苷受体拮抗剂（8-磺基苯基茶碱[8-So-PT]）联合使用L-PIA进行的MAC实验表明，其涉及中枢机制。在氟烷麻醉的大鼠中，所有脑区在给予L-PIA后去甲肾上腺素能神经传递均减弱。这些数据表明，急性L-PIA处理会降低中枢去甲肾上腺素能神经传递，这可能是降低氟烷剂量以达到麻醉终点（对氟烷的麻醉反应）的机制。