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大鼠膈下迷走神经电刺激产生的镇痛作用的定量表征及脊髓底物

Quantitative characterization and spinal substrates of antinociception produced by electrical stimulation of the subdiaphragmatic vagus in rats.

作者信息

Thurston Cindy L, Randich Alan

机构信息

Department of Psychology University of Iowa, Iowa City, IA 52242 U.S.A. Cardiovascular Research Center, University of Iowa, Iowa City, IA 52242 U.S.A.

出版信息

Pain. 1991 Feb;44(2):201-209. doi: 10.1016/0304-3959(91)90138-N.

Abstract

Physiological, chemical or electrical activation of vagal afferents produces antinociception in rats. The present study examined the effects of electrical stimulation of the subdiaphragmatic vagus (SDV) on the nociceptive tail-flick reflex, arterial blood pressure, and heart rate in rats lightly anesthetized with pentobarbital sodium. The intensity of SDV stimulation (20 Hz, 2 msec) necessary to inhibit the tail-flick reflex to a 10 sec cut-off latency for 3 consecutive trials was defined as the threshold to produce antinociception. Electrical stimulation of the SDV suppressed the tail-flick reflex in a linear, intensity-dependent manner. In addition, the threshold varied as a function of either the frequency or the pulse width of SDV stimulation, such that decreases in either frequency or pulse width, from 20 Hz and 2 msec, respectively, systematically increased the threshold current necessary to produce antinociception. SDV stimulation also produced modest decreases in heart rate (HR), but arterial blood pressure (ABP) responses were highly variable in both the magnitude and direction of change. Intrathecal administration of 30 micrograms of the serotonergic receptor antagonist methysergide significantly increased the threshold for antinociception produced by SDV stimulation from 80 to 938.8 microA, whereas 15 micrograms of methysergide had no significant effect. Intrathecal administration of saline, 30 micrograms of naloxone, or 30 micrograms of phentolamine had no significant effect on the threshold of SDV stimulation required to produce antinociception. Systemic administration of naloxone (4 mg/kg i.p. or i.v.) also had no effect on the antinociceptive threshold. Intrathecal administration of these receptor antagonists had no significant effect on the ABP and HR responses produced by electrical stimulation of the SDV at the threshold intensity producing antinociception.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

迷走神经传入纤维的生理、化学或电激活可在大鼠中产生抗伤害感受作用。本研究检测了膈下迷走神经(SDV)电刺激对用戊巴比妥钠轻度麻醉的大鼠伤害性甩尾反射、动脉血压和心率的影响。将连续3次试验中抑制甩尾反射至10秒截止潜伏期所需的SDV刺激强度(20赫兹,2毫秒)定义为产生抗伤害感受的阈值。SDV电刺激以线性、强度依赖性方式抑制甩尾反射。此外,阈值随SDV刺激的频率或脉冲宽度而变化,即分别从20赫兹和2毫秒降低频率或脉冲宽度会系统性地增加产生抗伤害感受所需的阈值电流。SDV刺激还使心率(HR)适度降低,但动脉血压(ABP)反应在变化幅度和方向上都高度可变。鞘内注射30微克5-羟色胺能受体拮抗剂麦角新碱可使SDV刺激产生抗伤害感受的阈值从80微安显著增加至938.8微安,而15微克麦角新碱则无显著影响。鞘内注射生理盐水、30微克纳洛酮或30微克酚妥拉明对产生抗伤害感受所需的SDV刺激阈值无显著影响。全身注射纳洛酮(4毫克/千克,腹腔注射或静脉注射)对抗伤害感受阈值也无影响。在产生抗伤害感受的阈值强度下,鞘内注射这些受体拮抗剂对SDV电刺激产生的ABP和HR反应无显著影响。(摘要截断于250字)

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