Inoue T, Ito Y, Takeda K
J Physiol. 1984 Apr;349:553-70. doi: 10.1113/jphysiol.1984.sp015173.
In an attempt to elucidate the possible roles of endogenous prostaglandins on the neuro-effector transmission in the dog trachea, effects of a prostaglandin antagonist (1-acetyl-2-[8-chloro-10, 11- dihydrobenz (b.f) (1.4) oxazepine-10-carbonyl]hydrazine (SC-19220] on the electrical and mechanical properties of smooth muscle cells and on neuro-effector transmission in the smooth muscle layer were studied by means of micro-electrode, double sucrose-gap, and tension recording methods. The levels of prostaglandins in the perfusate from the dog tracheal tissue were also determined using radioimmunoassay. Excitatory junction potentials (e.j.p.s) and twitch tension evoked by electrical field stimulation with short pulse duration (50-100 microseconds), which were abolished by tetrodotoxin (10(-7) M) or atropine (5 X 10(-6) M), showed gradual and continuous reduction in amplitude during superfusion with normal Krebs solution. Reduction in the amplitude of e.j.p.s occurred with no change in the membrane potential or membrane input resistance. SC-19220 (3.1 X 10(-5) M) did not modify the membrane potential, membrane input resistance or the sensitivity to acetylcholine of the smooth muscle cells. Yet, with application of SC-19220 (3.1 X 10(-6) M), gradual and continuous reductions in the amplitude of e.j.p.s and twitch contractions were no longer observed. With an increased concentration (3.1 X 10(-5) M), e.j.p.s and twitch contractions with a constant amplitude were obtained after the initial increase in the amplitude. When the amplitude of twitch contractions was stabilized by treatment with indomethacin (10(-5) M), low concentrations (10(-12) to 10(-10) M) of prostaglandin E2 (PGE2) or prostaglandin F2 alpha (10(-8) to 10(-6) M) markedly suppressed the amplitude of the twitch contractions. In some muscle preparations (ten out of twenty-two preparations examined), SC-19220 (3.1 X 10(-6) to 3.1 X 10(-5) M) produced a sustained contraction of the muscle, which was suppressed by atropine (5 X 10(-6) M) or PGE2 (10(-8) M). Following pre-treatment of the tissue with atropine (5 X 10(-6) M), SC-19220 did not evoke contracture. In the resting condition, 10-40 ng g-1 wet wt. tissue min-1 PGE or PGF was released into the perfusate from the tracheal muscle tissue of the control dog.(ABSTRACT TRUNCATED AT 400 WORDS)
为了阐明内源性前列腺素在犬气管神经效应器传递中的可能作用，采用微电极、双蔗糖间隙和张力记录方法，研究了前列腺素拮抗剂（1-乙酰基-2-[8-氯-10,11-二氢苯并(b.f)(1.4)恶唑嗪-10-羰基]肼(SC-19220)）对平滑肌细胞电和机械特性以及平滑肌层神经效应器传递的影响。还使用放射免疫测定法测定了犬气管组织灌流液中前列腺素的水平。由短脉冲持续时间（50-100微秒）的电场刺激诱发的兴奋性接头电位（e.j.p.s）和抽搐张力，可被河豚毒素（10(-7)M）或阿托品（5×10(-6)M）消除，在正常Krebs溶液灌流期间，其幅度逐渐持续降低。e.j.p.s幅度降低时，膜电位或膜输入电阻无变化。SC-19220（3.1×10(-5)M）未改变平滑肌细胞的膜电位、膜输入电阻或对乙酰胆碱的敏感性。然而，应用SC-19220（3.1×10(-6)M）后，不再观察到e.j.p.s幅度和抽搐收缩的逐渐持续降低。浓度增加（3.1×10(-5)M）时，在幅度最初增加后，可获得幅度恒定的e.j.p.s和抽搐收缩。当用吲哚美辛（10(-5)M）处理使抽搐收缩幅度稳定后，低浓度（10(-12)至10(-10)M）的前列腺素E2（PGE2）或前列腺素F2α（10(-8)至10(-6)M）可显著抑制抽搐收缩幅度。在一些肌肉标本中（检查的22个标本中有10个），SC-19220（3.1×10(-6)至3.1×10(-5)M）可使肌肉产生持续收缩，该收缩可被阿托品（5×10(-6)M）或PGE2（10(-8)M）抑制。用阿托品（5×10(-6)M）预处理组织后，SC-19220未诱发挛缩。在静息状态下，对照犬气管肌肉组织有10-40 ng g-1湿重·组织·分钟-1的PGE或PGF释放到灌流液中。（摘要截断于400字）
