Downes H, Gerber N, Hirshman C A
Br J Anaesth. 1980 Sep;52(9):873-8. doi: 10.1093/bja/52.9.873.
The protection against bronchospasm afforded by infusions of lignocaine was tested in dogs anaesthetized with thiamylal by challenge with aerosols of citric acid (CAA) or ascaris antigen (AAA). During the infusion of lignocaine, the response to CAA was blocked or markedly attenuated, but AAA still elicited a large increase in pulmonary resistance (RL). In untreated dogs, CAA increased RL from 0.14 +/- 0.05 (mean +/- SEM) kPa litre-1 s to 1.09 +/- 0.18, whereas in dogs treated with lignocaine, RL was 0.19 +/- 0.09 before challenge with CAA and 0.44 +/- 0.13 after challenge. AAA increased RL from 0.14 +/- 0.06 kPa litre-1 s to 3.01 +/- 0.65 in untreated dogs, and from 0.34 +/- 0.10 kPa litre-1 to 1.85 +/- 0.69 in dogs treated with lignocaine. Blood concentrations of lignocaine were 1.5 +/- 0.3 and 2.5 +/- 0.6 microgram ml-1 during challenge with CAA and AAA, respectively. We conclude that lignocaine, at blood concentrations which will reduce the risk of cardiac arrhythmia, markedly reduces reflex bronchonconstriction, but has relatively little effect on that initiated by allergic mediators.
通过用硫喷妥钠麻醉犬,并用柠檬酸气雾剂(CAA)或蛔虫抗原(AAA)进行激发试验,来测试输注利多卡因对支气管痉挛的保护作用。在输注利多卡因期间,对CAA的反应被阻断或明显减弱,但AAA仍引起肺阻力(RL)大幅增加。在未治疗的犬中,CAA使RL从0.14±0.05(均值±标准误)kPa·升⁻¹·秒增加到1.09±0.18,而在接受利多卡因治疗的犬中,在CAA激发前RL为0.19±0.09,激发后为0.44±0.13。在未治疗的犬中,AAA使RL从0.14±0.06 kPa·升⁻¹·秒增加到3.01±0.65,在接受利多卡因治疗的犬中,从0.34±0.10 kPa·升⁻¹增加到1.85±0.69。在CAA和AAA激发期间,利多卡因的血药浓度分别为1.5±0.3和2.5±0.6微克·毫升⁻¹。我们得出结论,在能降低心律失常风险的血药浓度下,利多卡因可显著降低反射性支气管收缩,但对由过敏介质引发的支气管收缩影响相对较小。