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速激肽在豚鼠死后空气通气诱导的支气管收缩中的作用

The role of tachykinins in air ventilation-induced bronchoconstriction in postmortem guinea pigs.

作者信息

Shi M X, Lai Y L

机构信息

Pharmacology and Experimental Therapeutics Division, University of Kentucky College of Pharmacy, Lexington.

出版信息

Respir Physiol. 1990 Jul;81(1):75-86. doi: 10.1016/0034-5687(90)90071-6.

DOI:10.1016/0034-5687(90)90071-6
PMID:2120759
Abstract

To investigate the relationship between tachykinins and air ventilation-induced airway constriction after heart ligation, 26 guinea pigs were divided into three groups: Group 1, control (n = 15); Group 2, tachykinin depletion via pretreatment with capsaicin (n = 7); and Group 3, isocapnic ventilation (n = 4). To examine the age effect, the first two groups were further separated into two subgroups: young (n = 12) and mature (n = 10). Animals were anesthetized with pentobarbital, sternotomized and artificially ventilated with room air or with 5% CO2 gas mixture. Before (baseline) and after heart ligation, tidal volume and transpulmonary pressure (Ptp) were recorded during ventilation, and the maximal expiratory flow-volume curve was periodically obtained. Minimal volume (lung volume at Ptp = 0) was determined by neon dilution. Within 30 min after heart ligation in the control group, air ventilation significantly decreased dynamic compliance, vital capacity, peak maximal expiratory flow, maximal expiratory flow at 50% total lung capacity, and forced expiratory volume in 0.2 sec. Tachykinin depletion significantly prevented, whereas isocapnic (5% CO2) ventilation failed to alter, the above changes. Young and mature subgroups showed similar results. Our data indicate that air ventilation after heart ligation induced severe airway constriction and that this bronchoconstriction can be prevented by tachykinin depletion.

摘要

为了研究速激肽与心脏结扎后通气诱导的气道收缩之间的关系,将26只豚鼠分为三组:第1组为对照组(n = 15);第2组通过用辣椒素预处理使速激肽耗竭(n = 7);第3组为等碳酸通气组(n = 4)。为了研究年龄的影响,前两组进一步分为两个亚组:年轻组(n = 12)和成熟组(n = 10)。动物用戊巴比妥麻醉,开胸并使用室内空气或5%二氧化碳混合气体进行人工通气。在心脏结扎前(基线)和结扎后,记录通气过程中的潮气量和跨肺压(Ptp),并定期获取最大呼气流量-容积曲线。最小容积(Ptp = 0时的肺容积)通过氖稀释法测定。在对照组心脏结扎后30分钟内,通气显著降低了动态顺应性、肺活量、最大呼气流量峰值、肺总量50%时的最大呼气流量以及0.2秒用力呼气量。速激肽耗竭可显著预防上述变化,而等碳酸(5%二氧化碳)通气未能改变这些变化。年轻亚组和成熟亚组显示出相似的结果。我们的数据表明,心脏结扎后的通气会诱发严重的气道收缩,并且这种支气管收缩可通过速激肽耗竭来预防。

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