Groeben H, Schwalen A, Irsfeld S, Tarnow J, Lipfert P, Hopf H B
Institut für Anaesthesiologie, Heinrich-Heine Universität, Düsseldorf, Germany.
Anesthesiology. 1994 Oct;81(4):868-74. doi: 10.1097/00000542-199410000-00014.
The functional relevance of an intact pulmonary sympathetic innervation for airway resistance is unknown. We therefore evaluated whether or not pulmonary sympathetic denervation by thoracic epidural anesthesia decreases the threshold of an inhalational provocation with acetylcholine in 20 patients with documented bronchial hyperreactivity scheduled for elective upper abdominal or thoracic surgery.
Baseline inhalational provocation with acetylcholine was performed 2-4 days before surgery. The acetylcholine threshold concentration for a hyperreactivity response (i.e., for a 20% decrease in forced expiratory volume in 1 s and a 100% increase in total respiratory resistance by oscillometry) was determined. On the day of surgery a second inhalative provocation with acetylcholine was performed 45 min after the patients had received 6-8 ml epidural bupivacaine 0.75% (n = 10), intravenous bupivacaine (1.2 mg.min-1, n = 6), or 6-8 ml epidural saline (n = 4). The acetylcholine threshold concentration for a hyperreactive response was again determined. We also measured vital capacity, forced expiratory volume in 1 s as a percentage of vital capacity, spread of sensory blockade (pin prick), skin temperature on hand and foot (telethermography).
During thoracic epidural anesthesia, C4-T8 skin temperature increased significantly on hand and foot indicating widespread sympathetic blockade including the lungs. Compared to values obtained immediately before pulmonary sympathetic blockade, forced expiratory volume in 1 s as a percentage of vital capacity, and total respiratory resistance by oscillometry remained unchanged, while vital capacity decreased. Compared to baseline the acetylcholine threshold concentration for the hyperreactive response increased threefold after epidural as well as after intravenous bupivacaine. Epidural saline evoked no directional changes in the acetylcholine threshold concentration.
We conclude that in patients with bronchial hyperreactivity 1. blockade of pulmonary sympathetic innervation seems to be of no relevance for airway resistance and 2. both epidural and intravenous bupivacaine substantially attenuate the response to an inhalational provocation with acetylcholine.
完整的肺交感神经支配对气道阻力的功能相关性尚不清楚。因此，我们评估了在20例计划行择期上腹部或胸部手术且有支气管高反应性记录的患者中，胸段硬膜外麻醉进行肺交感神经去神经支配是否会降低乙酰胆碱吸入激发试验的阈值。
在手术前2 - 4天进行乙酰胆碱基线吸入激发试验。确定高反应性反应的乙酰胆碱阈值浓度（即1秒用力呼气量降低20%且通过振荡法测定的总呼吸阻力增加100%时的浓度）。手术当天，在患者接受6 - 8毫升0.75%的硬膜外布比卡因（n = 10）、静脉注射布比卡因（1.2毫克·分钟⁻¹，n = 6）或6 - 8毫升硬膜外生理盐水（n = 4）后45分钟，再次进行乙酰胆碱吸入激发试验。再次确定高反应性反应的乙酰胆碱阈值浓度。我们还测量了肺活量、1秒用力呼气量占肺活量的百分比、感觉阻滞范围（针刺）、手足皮肤温度（远红外热成像）。
在胸段硬膜外麻醉期间，手足的C4 - T8皮肤温度显著升高，表明包括肺部在内的广泛交感神经阻滞。与肺交感神经阻滞前立即获得的值相比，1秒用力呼气量占肺活量的百分比以及通过振荡法测定的总呼吸阻力保持不变，而肺活量下降。与基线相比，硬膜外和静脉注射布比卡因后，高反应性反应的乙酰胆碱阈值浓度增加了三倍。硬膜外生理盐水未引起乙酰胆碱阈值浓度的定向变化。
我们得出结论，在支气管高反应性患者中，1. 肺交感神经支配的阻滞似乎与气道阻力无关；2. 硬膜外和静脉注射布比卡因均显著减弱对乙酰胆碱吸入激发试验的反应。
