Physiological and pharmacological response of canine bronchial smooth muscle in situ.

Physiological and pharmacological response of canine bronchial smooth muscle in situ.
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犬支气管平滑肌原位的生理和药理反应。

DOI:
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发表时间:
1983
期刊:
Journal of applied physiology: respiratory, environmental and exercise physiology
影响因子:
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通讯作者:
A. Leff
A. Leff
中科院分区:
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文献类型:
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作者:
S. Hendrix;N. Muñoz;A. Leff

文献摘要

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我们现场研究了 24 只狗的单个三级支气管中支气管平滑肌的等长反应。通过将 10(-5) mol 乙酰胆碱 (ACh) 重复注射到右支气管食管动脉中,对六只狗进行了长度-张力研究,并确定了允许最大收缩的静息张力 (30.6 +/- 6.9 g/cm) 和长度 (0.76 +/- 0.14 cm)。在另外八只狗中,用 10(-10) 至 10(-5) mol 动脉内 (ia) 乙酰胆碱获得剂量相关的支气管收缩。用1-1-二甲基-4-苯基哌嗪(DMPP)对右侧颈迷走神经进行超最大电刺激并刺激支气管副交感神经节,也引起支气管收缩。对ia ACh (28.5 +/- 1.7 g/cm)、超最大电刺激(15.2 +/- 1.1 g/cm)和ia DMPP (10.5 +/- 3.0 g/cm)的最大反应被ia剂量的阿托品(1-5微克/kg)阻断,不会改变气管中的交感神经松弛反应。在四只狗中,在用阿托品阻断胆碱能后,通过静脉(iv)推注DMPP来研究支气管对交感神经激活的反应。 DMPP(25微克/公斤静脉注射)引起9.5+/-2.2克/厘米的支气管松弛,这种松弛被2-4毫克/公斤静脉注射普萘洛尔完全阻断。在另外六只狗中,纯氮通气引起的缺氧导致支气管收缩,而迷走神经切断术、阿托品和六甲铵可阻止支气管收缩。我们报告了一种选择性测量单阻力支气管中支气管平滑肌反应的灵敏方法。这种制剂保留了区域神经支配和循环,并允许在原位进行选择性生理刺激。
We studied the isometric response of bronchial smooth muscle in a single third-order bronchus of 24 dogs in situ. Length-tension studies were performed in six dogs by repeated injection of 10(-5) mol acetylcholine (ACh) into the right bronchoesophageal artery, and the resting tension (30.6 +/- 6.9 g/cm) and length (0.76 +/- 0.14 cm) permitting maximal contraction were determined. In eight other dogs, dose-related bronchial contraction was obtained with 10(-10) to 10(-5) mol intra-arterial (ia) ACh. Supramaximal electrical stimulation of the right cervical vagus nerve and bronchial parasympathetic ganglion stimulation with ia 1-1-dimethyl-4-phenylpiperazinium (DMPP) also caused bronchial contraction. The maximal response to ia ACh (28.5 +/- 1.7 g/cm), supramaximal electrical stimulation (15.2 +/- 1.1 g/cm), and ia DMPP (10.5 +/- 3.0 g/cm) was blocked by an ia dose of atropine (1-5 micrograms/kg) that did not alter the sympathetic relaxation response in the trachea. In four dogs, the bronchial response to sympathetic activation was studied by intravenous (iv) bolus injection of DMPP after cholinergic blockade with atropine. DMPP (25 micrograms/kg iv) caused 9.5 +/- 2.2 g/cm bronchial relaxation, which was blocked completely by 2-4 mg/kg iv propranolol. In six other dogs, hypoxia induced by ventilation with pure nitrogen caused bronchial contraction, which was blocked by vagotomy, atropine, and hexamethonium. We report a sensitive method for selective measurement of bronchial smooth muscle response in a single resistance bronchus. This preparation preserves regional innervation and circulation and permits selective physiological stimulation in situ.