Munoz N M, Shioya T, Murphy T M, Primack S, Dame C, Sands M F, Leff A R
J Appl Physiol (1985). 1986 Sep;61(3):1173-9. doi: 10.1152/jappl.1986.61.3.1173.
We studied the effect of the thromboxane mimetic U-46619 on tracheal smooth muscle contraction caused by bilateral stimulation of the vagus nerves in 14 mongrel dogs in situ. The parasympathetic contractile response was studied isometrically after beta-adrenergic blockade with 2 mg/kg iv propranolol plus 20 micrograms X kg-1 X min-1 continuous intravenous infusion and blockade of endogenous prostaglandin synthesis with 5 mg/kg iv indomethacin. An initial frequency-response curve was generated by electrical stimulation of the caudal ends of cut cervical vagi over the range of frequencies 2-25 Hz (constant 25 V) at 15-s intervals. In five dogs, 10(-10) to 10(-8) mol of the thromboxane mimetic (15S)-hydroxyl-11 alpha,9 alpha-(epoxymethano)prosta-5Z,13E-dienoic acid (U-46619) was injected selectively into the tracheal arterial circulation, causing a transient contractile response (less than or equal to 10 g/cm). Additional frequency response studies were generated 7 min before and 1, 15, 30, 45, and 60 min after U-46619. Substantial augmentation of tracheal contraction to efferent vagal stimulation was observed after U-46619 for all frequencies greater than 4 Hz (P less than 0.02). Augmentation of vagally mediated contraction was not observed in four other dogs after equivalent tracheal contraction was elicited without U-46619. Similarly, in four separate dogs, augmentation of tracheal contraction was not observed when acetylcholine was given instead of vagal stimulation after U-46619. We conclude that the thromboxane analogue, U-46619, causes augmentation of tracheal contractile response induced by efferent vagus nerve stimulation. Potentiation is caused by a prejunctional action of U-46619 and is not induced by nonspecific precontraction with another agonist.
我们在14只杂种犬原位研究了血栓素类似物U - 46619对双侧迷走神经刺激所致气管平滑肌收缩的影响。在用2mg/kg静脉注射普萘洛尔加20μg·kg⁻¹·min⁻¹持续静脉输注进行β - 肾上腺素能阻滞以及用5mg/kg静脉注射吲哚美辛阻滞内源性前列腺素合成后，以等长方式研究副交感神经收缩反应。通过在2 - 25Hz频率范围（恒定25V）以15秒间隔电刺激切断的颈迷走神经尾端来生成初始频率 - 反应曲线。在5只犬中，将10⁻¹⁰至10⁻⁸mol的血栓素类似物（15S） - 羟基 - 11α，9α - （环氧亚甲基）前列腺 - 5Z，13E - 二烯酸（U - 46619）选择性注入气管动脉循环，引起短暂收缩反应（小于或等于10g/cm）。在U - 46619注射前7分钟以及注射后1、15、30、45和60分钟进行额外的频率反应研究。对于所有大于4Hz的频率，在U - 46619注射后观察到气管对传出迷走神经刺激的收缩明显增强（P小于0.02）。在另外4只犬中，在未使用U - 46619引发同等气管收缩后，未观察到迷走神经介导的收缩增强。同样，在4只单独的犬中，在U - 46619注射后给予乙酰胆碱代替迷走神经刺激时，未观察到气管收缩增强。我们得出结论，血栓素类似物U - 46619可导致传出迷走神经刺激引起的气管收缩反应增强。增强作用是由U - 46619的节前作用引起的，而非由另一种激动剂的非特异性预收缩诱导。
