Bronchial circulatory reversal of methacholine-induced airway constriction.
Bronchial circulatory reversal of methacholine-induced airway constriction.
复制标题
乙酰甲胆碱引起的气道收缩的支气管循环逆转。
DOI：
10.1152/jappl.1990.69.4.1220
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发表时间：
1990
影响因子：
3.3
通讯作者：
W. Mitzner
中科院分区：
文献类型：
--
作者：
E. Wagner;W. Mitzner
虽然支气管循环在清除支气管活性物质中的作用经常被提出，但实验证据有限。在这项研究中，我们确定了支气管血流量(QBA)在乙酰甲胆碱(MCH)诱导的支气管收缩中恢复的重要性。10只戊巴比妥钠麻醉机械通气绵羊，经气管插管注入0.7mL.min~(-1)kg~(-1)的股动脉血。MCH按递增浓度(10(-7)~10(-5)M)直接注入支气管动脉。恒定QBA时，MCH输注引起的气道阻力呈浓度依赖性增加。然而，停用MCH后从气道狭窄中恢复的时间常数(TC)不依赖于MCH浓度或气道阻力增加的幅度。当QBA浓度为对照水平的50%、100%和200%时，当MCH浓度不变时，TC分别为44+/-6、25+/-2和24+/-2(SE)S。50%对照QBA时TC显著高于对照QBA(P<0.01)。因此，QBA的大小可以改变MCH引起的气道阻力增加的恢复时间进程。这些结果证明了QBA在逆转激动剂诱导的收缩中的重要性，并提示支气管循环受损可能参与了呼吸道高反应性的机制。
Although a role for the bronchial circulation in clearance of bronchoactive agents has been frequently proposed, experimental evidence is limited. In this study, we determined the importance of bronchial blood flow (QBA) in the recovery from methacholine-(MCh) induced bronchoconstriction. In 10 pentobarbital-anesthetized ventilated sheep, the bronchial branch of the bronchoesophageal artery was cannulated and perfused (0.7 ml.min-1.kg-1) with blood pumped from the femoral artery. MCh was infused directly into the bronchial artery at increasing concentrations (10(-7) to 10(-5) M). MCh infusion caused a concentration-dependent increase in airway resistance at constant QBA. However, the time constant of recovery (TC) from airway constriction after cessation of the MCh infusion was not dependent on the MCh concentration or the magnitude of the increases in airway resistance. When QBA was at 50, 100, and 200% of control level, with constant MCh concentration, TC was 44 +/- 6, 25 +/- 2, and 24 +/- 2 (SE) s at each flow level, respectively. TC at 50% of control QBA was significantly greater than at control QBA (P less than 0.01). Thus the magnitude of QBA can alter the time course of recovery from MCh-induced increases in airway resistance. These results document the importance of QBA in reversing agonist-induced constriction and suggest that an impaired bronchial circulation may contribute to the mechanism of airway hyperreactivity.