Dorward A J, Fisher B M, Frier B M, Thomson N C
Department of Respiratory Medicine, Western Infirmary, Glasgow.
Pulm Pharmacol. 1990;3(2):89-92. doi: 10.1016/0952-0600(90)90037-j.
The role of vagal mechanisms in the reversal of pharmacologically-induced bronchoconstriction by deep inspiration is unclear. We examined the effect of lung inflation on methacholine-induced bronchoconstriction in six patients with severe diabetic autonomic neuropathy compared with five patients with diabetes mellitus and normal tests of autonomic function. The effect of deep inspiration on bronchomotor tone was expressed as the ratio of maximal flow rates at 70% of expiratory vital capacity (V30) calculated from complete (V30(c)) and partial (V30(p)) flow-volume curves (V30(c)/V30(p)). In patients with autonomic neuropathy the mean (range) of this ratio was 1.31 (1.19-1.47) and was not significantly different from the control patients with a mean ratio of 1.69 (1.28-2.13). These results suggest that the reversal of methacholine-induced bronchoconstriction by a deep inspiration is not mediated via vagal nerves.
迷走神经机制在深吸气逆转药物诱导的支气管收缩中所起的作用尚不清楚。我们研究了肺扩张对6例严重糖尿病自主神经病变患者与5例自主神经功能测试正常的糖尿病患者中乙酰甲胆碱诱导的支气管收缩的影响。深吸气对支气管运动张力的影响以从完整(V30(c))和部分(V30(p))流量-容积曲线计算出的呼气肺活量70%时的最大流速比值(V30(c)/V30(p))来表示。自主神经病变患者中该比值的平均值(范围)为1.31(1.19 - 1.47),与平均比值为1.69(1.28 - 2.13)的对照患者相比无显著差异。这些结果表明,深吸气逆转乙酰甲胆碱诱导的支气管收缩并非通过迷走神经介导。