Canine bronchoconstriction, gas trapping, and hypoxia with methacholine.
Canine bronchoconstriction, gas trapping, and hypoxia with methacholine.
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乙酰甲胆碱可导致犬支气管收缩、气体滞留和缺氧。
DOI：
10.1152/jappl.1987.63.1.262
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发表时间：
1987
期刊：
影响因子：
--
通讯作者：
Wood,LD
中科院分区：
文献类型：
--
作者：
Breen,PH;Becker,LJ;Ruygrok,P;Mayers,I;Long,GR;Leff,A;Wood,LD
7只杂种狗（22.0±2.8 kg）被氯氯蔗糖和脲聚糖麻醉，并被心得安阻断-肾上腺素能阻滞，研究了静脉输注甲胆碱对其心肺功能的影响。在容积容积容积描记仪中，在基线和建立甲胆碱输注（0.1-1.0 mg X kg-1 X h-1）后25分钟进行生理测量。甲胺胆碱显著（P < 0.05）增加气道阻力（1.9 +/- 0.8 ~ 8.2 +/- 2.9 cmH2O X l - 1 X s），降低肺静态顺应性（84.7 +/- 18.5 ~ 48.2 +/- 9.4 ml/cmH2O），降低动脉PO2 (81 +/- 17 ~ 56 +/- 10 Torr)，降低血压（132 +/- 10 ~ 69 +/- 18 Torr）和心输出量（5.7 +/- 1.9 ~ 4.1 +/- 1.2 l/min）。在另外5只动物中，这些影响持续了80分钟的甲胆碱输注。在使用甲胆碱的最初25分钟内，所有动物的终末容积（容积置换克罗格肺活量计）均升高，表明功能残气量从997 +/- 115 ml增加到1623 +/- 259 ml （P < 0.0005）。肺压力-容积曲线分析显示，总肺活量无变化，但残气量从489 +/- 168 ml增加到1106 +/- 216 ml （P < 0.001）。因此，甲胆碱引起了617毫升的气体捕获，而波义耳定律原理没有检测到，这可能是因为气体在高肺压下被捕获。我们认为，静脉注射甲基苯丙胺引起的犬支气管收缩，引起气体潴留和缺氧，可能是一种有用的哮喘临床状态动物模型。
The effects of an intravenous methacholine infusion on cardiovascular-pulmonary function were measured in seven mongrel dogs (22.0 +/- 2.8 kg), anesthetized with chloralose and urethan and beta-adrenergically blocked with propranolol. In a volume-displacement plethysmograph, physiological measurements were made at base line and 25 min after establishing a methacholine infusion (0.1–1.0 mg X kg-1 X h-1). Methacholine significantly (P less than 0.05) increased airways resistance (1.9 +/- 0.8 to 8.2 +/- 2.9 cmH2O X l–1 X s), decreased static lung compliance (84.7 +/- 18.5 to 48.2 +/- 9.4 ml/cmH2O), depressed arterial PO2 (81 +/- 17 to 56 +/- 10 Torr), and lowered blood pressure (132 +/- 10 to 69 +/- 18 Torr) and cardiac output (5.7 +/- 1.9 to 4.1 +/- 1.2 l/min). These effects persisted during a further 80 min of methacholine infusion conducted in five of the animals. During the initial 25-min period of methacholine, the end-expired volume (volume-displacement Krogh spirometer) rose in all animals, indicating an increase in functional residual capacity from 997 +/- 115 to 1,623 +/- 259 ml (P less than 0.0005). Analysis of pulmonary pressure-volume curves revealed no change in total lung capacity but an increase in residual volume from 489 +/- 168 to 1,106 +/- 216 ml (P less than 0.001). Thus methacholine caused 617 ml of gas trapping, which was not detected by the Boyle's law principle, presumably because gas was trapped at high transpulmonary pressure. We suggest that intravenous methacholine-induced canine bronchoconstriction, which causes gas trapping and hypoxia, may be a useful animal model of clinical status asthmaticus.