Breen P H, Becker L J, Ruygrok P, Mayers I, Long G R, Leff A, Wood L D
J Appl Physiol (1985). 1987 Jul;63(1):262-9. doi: 10.1152/jappl.1987.63.1.262.
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.
在7只杂种犬（体重22.0±2.8千克）身上测量了静脉输注乙酰甲胆碱对心肺功能的影响。这些犬用氯醛糖和乌拉坦麻醉，并使用普萘洛尔进行β-肾上腺素能阻滞。在容积置换式体积描记器中，在基线以及建立乙酰甲胆碱输注（0.1 - 1.0毫克×千克⁻¹×小时⁻¹）25分钟后进行生理测量。乙酰甲胆碱显著（P＜0.05）增加气道阻力（从1.9±0.8增加至8.2±2.9厘米水柱×升⁻¹×秒），降低静态肺顺应性（从84.7±18.5降至48.2±9.4毫升/厘米水柱），降低动脉血氧分压（从81±17降至56±10托），并降低血压（从132±10降至69±18毫米汞柱）和心输出量（从5.7±1.9降至4.1±1.2升/分钟）。在其中5只动物中进行的进一步80分钟乙酰甲胆碱输注期间，这些效应持续存在。在乙酰甲胆碱输注的最初25分钟内，所有动物的呼出末容积（容积置换式克罗格肺量计）均升高，表明功能残气量从997±115毫升增加至1,623±259毫升（P＜0.0005）。肺压力 - 容积曲线分析显示肺总量无变化，但残气量从489±168毫升增加至1,106±216毫升（P＜0.001）。因此，乙酰甲胆碱导致617毫升气体潴留，这未被玻意耳定律原理检测到，推测是因为气体在高跨肺压下潴留。我们认为静脉注射乙酰甲胆碱诱导的犬支气管收缩，会导致气体潴留和缺氧，可能是临床哮喘状态的一种有用动物模型。
