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豚鼠输精管嘌呤能神经源性收缩的消退:可能机制的分析。

The fade of the purinergic neurogenic contraction of the guinea-pig vas deferens: analysis of possible mechanisms.

作者信息

Driessen B, von Kügelgen I, Bültmann R, Elrick D B, Cunnane T C, Starke K

机构信息

Pharmakologisches Institut, Universität Freiburg, Germany.

出版信息

Naunyn Schmiedebergs Arch Pharmacol. 1994 Nov;350(5):482-90. doi: 10.1007/BF00173017.

Abstract

The purinergic response of the guinea-pig vas deferens to long trains of pulses at high frequency consists of an initial twitch followed by a much lower plateau. Mechanical, neurochemical and electrophysiological techniques were used to examine the reason for the fade. Mechanical measurements. In tissues stimulated by trains of 180 pulses/10 Hz and treated with prazosin to suppress the noradrenergic contraction component, the response to alpha, beta-methylene ATP and to exogenous ATP was as high during the secondary plateau of the purinergic neurogenic contraction as it was outside electrical stimulation periods; the response to 50 pulses/100 Hz was also unchanged during the low plateau. The plateau was not increased by reactive blue 2,8-(p-sulphophenyl)theophylline, propranolol or capsaicin. Neurochemical measurements. In tissues preincubated with [3H]-noradrenaline, electrical stimulation elicited an overflow of tritium and of ATP. In the absence of drugs as well as in the presence of prazosin and suramin to suppress contractions, the overflow of tritium per pulse decreased slightly in the course of trains of 90 pulses/10 Hz; the overflow of ATP per pulse decreased to a greater extent on average, but the decrease was not statistically significant. In the presence of prazosin and nifedipine, also to suppress contractions, the overflow of tritium per pulse again decreased slightly in the course of trains of 105 pulses/10 Hz, but the overflow of ATP per pulse if anything tended to increase. Electrophysiological measurements.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

豚鼠输精管对高频长串脉冲的嘌呤能反应包括一个初始抽搐,随后是一个低得多的平台期。采用机械、神经化学和电生理技术来研究消退的原因。机械测量。在用哌唑嗪处理以抑制去甲肾上腺素能收缩成分的情况下,对180个脉冲/10Hz的串刺激的组织中,在嘌呤能神经源性收缩的二次平台期,对α,β-亚甲基ATP和外源性ATP的反应与电刺激期外一样高;对50个脉冲/100Hz的反应在低平台期也没有变化。反应性蓝2、8-(对磺苯基)茶碱、普萘洛尔或辣椒素均未使平台期增加。神经化学测量。在用[3H]-去甲肾上腺素预孵育的组织中,电刺激引起氚和ATP的溢出。在无药物以及存在哌唑嗪和苏拉明以抑制收缩的情况下,在90个脉冲/10Hz的串刺激过程中,每个脉冲的氚溢出略有下降;每个脉冲的ATP溢出平均下降幅度更大,但下降无统计学意义。在存在哌唑嗪和硝苯地平(同样用于抑制收缩)的情况下,在105个脉冲/10Hz的串刺激过程中,每个脉冲的氚溢出再次略有下降,但每个脉冲的ATP溢出反而有增加的趋势。电生理测量。(摘要截断于250字)

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