Distribution of airway contractile responses within the major diameter bronchi during exogenous bronchoconstriction.

Distribution of airway contractile responses within the major diameter bronchi during exogenous bronchoconstriction.
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外源性支气管收缩期间大直径支气管内气道收缩反应的分布。

DOI:
10.1164/arrd.1987.135.5.1105
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发表时间:
1987
期刊:
The American review of respiratory disease
影响因子:
--
通讯作者:
Leff,AR
Leff,AR
中科院分区:
--
文献类型:
--
作者:
Shioya,T;Solway,J;Munoz,NM;Mack,M;Leff,AR

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在12只接受迷走神经切断术和β-肾上腺素能阻滞的杂种狗中,用乙酰甲胆碱(MCh)、前列腺素F2α(PGF 2 α)、去甲肾上腺素(NE)和血栓素模拟物U-46619 [(15 S)-羟基-11 α,9 α-(环氧甲氨基)前列腺-5Z,13 E-二烯酸]进行外源性支气管收缩时,通过钽支气管造影研究了0 - 6代气道内支气管收缩反应的分布。以随机顺序产生对每种激动剂的剂量-反应曲线,并且在静脉内(iv)输注后每种剂量的激动剂的反应的平台处获得钽支气管造影和肺阻力(RI)和动态肺顺应性(Cdyn)的同时测量。在5 × 10− 7 mol/kg剂量下,NE(β-肾上腺素能阻滞后)导致Rl中基线水平升高至254 ± 27.3%,PGF 2 α升高至368 ± 50.0%,U-46619升高至522 ± 98.5%,MCh升高至1,204 ± 173%。然而,对于每种激动剂,大直径气道内的气道直径变化差异很大。乙酰甲胆碱引起所有气道的实质性收缩。NE和U-46619在第0代或第1代中均未引起显著的气道狭窄,尽管两种激动剂在第6代气道中均引起> 30%的狭窄。前列腺素F2α(5 × 10− 7 mol/kg)导致Rl增加> 350%;然而,这伴随着第1代至第4代气道直径增加约10%(扩张),第6代气道狭窄约25%。我们证明了α-肾上腺素能激动剂和血栓素类似物在肺的中央气道原位引起大量的支气管收缩。我们还证明,对于RI的可比变化,支气管收缩反应在大直径支气管内的分布对于每种收缩激动剂的每个气道都有很大的不同。
The distribution of bronchoconstrictor responses within airway generations zero to 6 was studied by tantalum bronchography during exogenous bronchoconstriction with methacholine (MCh), prostaglandin F2α(PGF2α), norepinephrine (NE), and the thromboxane mimetic U-46619 [(15S)-hydroxyl-11α,9α-(epoxymethano)prosta-5Z,13E-dienoic acid] in 12 mongrel dogs undergoing vagotomy and beta-adrenergic blockade. Dose-response curves to each agonist were generated in random order, and tantalum bronchograms and simultaneous measurements of pulmonary resistance (Rl) and dynamic pulmonary compliance (Cdyn) were obtained at the plateau of the response of each dose of agonist after intravenous (iv) infusion. At 5 × 10−7mol/kg, NE (after β-adrenergic blockade) caused an increase to 254 ± 27.3%, PGF2αto 368 ± 50.0%, U-46619 to 522 ± 98.5%, and MCh to 1,204 ± 173% of baseline in Rl. However, airway diameter changes within the major diameter airways varied substantially for each agonist. Methacholine caused substantial contraction in all airways. Neither NE nor U-46619 caused significant airway narrowing in generations zero or 1, although both agonists caused > 30% narrowing in sixth generation airways. Prostaglandin F2α(5 × 10−7mol/kg) cause an increase in Rlof > 350%; however, this was accompanied by an ∼10%increase(dilation) in airway diameter in generation 1 through generation 4 airways and an approximate 25%narrowingin generation 6 airways. We demonstrate that both alpha-adrenergic agonists and thromboxane analog cause substantial bronchoconstriction in situ in the central airways of the lung. We also demonstrate that for comparable changes in Rl, the distribution of bronchoconstrictor responseswithinthe major diameter bronchi varies substantially for each airway with each contractile agonist.
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