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大鼠输精管前列腺端强直后抽搐抑制的研究。

A study of the post-tetanic twitch depression at the prostatic end of the rat vas deferens.

作者信息

Amobi N I, Smith I C

出版信息

Pflugers Arch. 1987 May;408(6):628-33. doi: 10.1007/BF00581166.

Abstract

The effects of different drugs on the post-tetanic twitch responses of the prostatic end of the isolation rat vas deferens were examined. Following repetitive field stimulation (4-5 Hz for 40-60 s), the post-tetanic twitches (0.2-0.5 Hz) were depressed relative to the steady-state pretetanic twitches. Maximum post-tetanic twitch depression (PTD) occurred 15-30 s after the tetanic stimulation. The PTD was not reversed but deepened and prolonged by the presynaptic alpha 2-adrenoceptor antagonists idazoxan (RX781094) or yohimbine (10(-7) M) alone or combined with the neuronal uptake blocker, desipramine (10(-6) M). The PTD was insensitive to the beta-adrenoceptor blocker, propranolol (10(-6) M), the P1-purinoceptor antagonist, 8-phenyltheophylline (10(-5) M) or the prostaglandin E synthesis inhibitor, indomethacin (10(-6) M). Pre- and post-tetanic contractions to superfused noradrenaline (NA), adenosine 5'-triphosphate (ATP), or beta, gamma-methylene ATP (beta, gamma-mATP) (bolus injections into superfusate, 1-8 X 10(-5) M) were not significantly (p less than 0.01) different. The PTD was absent in high magnesium (6.2-11.2 mM) solutions. These results are consistent with the PTD having an intrinsic presynaptic origin. They are discussed in relation to stimulation-induced modulation of transmitter release.

摘要

研究了不同药物对离体大鼠输精管前列腺端强直后抽搐反应的影响。在重复场刺激(4 - 5Hz,持续40 - 60秒)后,强直后抽搐(0.2 - 0.5Hz)相对于强直前稳态抽搐受到抑制。强直刺激后15 - 30秒出现最大强直后抽搐抑制(PTD)。单独使用突触前α2 - 肾上腺素能拮抗剂咪唑克生(RX781094)或育亨宾(10^(-7)M),或与神经元摄取阻滞剂地昔帕明(10^(-6)M)联合使用时,PTD并未逆转,反而加深和延长。PTD对β - 肾上腺素能阻滞剂普萘洛尔(10^(-6)M)、P1 - 嘌呤受体拮抗剂8 - 苯基茶碱(10^(-5)M)或前列腺素E合成抑制剂吲哚美辛(10^(-6)M)不敏感。对灌流的去甲肾上腺素(NA)、腺苷5'-三磷酸(ATP)或β,γ - 亚甲基ATP(β,γ - mATP)(向灌流液中推注,1 - 8×10^(-5)M)的强直前和强直后收缩无显著差异(p < 0.01)。在高镁(6.2 - 11.2mM)溶液中不存在PTD。这些结果与PTD具有内在的突触前起源一致。并就刺激诱导的递质释放调节进行了讨论。

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