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迷走神经和交感神经去神经支配在油酸诱导的肺水肿发生中的作用

Vagal and sympathetic denervation in the development of oleic acid-induced pulmonary edema.

作者信息

Du H L, Yamada Y, Orii R, Suwa K, Hanaoka K

机构信息

Department of Anesthesiology, Faculty of Medicine, University of Tokyo, Japan.

出版信息

Respir Physiol. 1997 Mar;107(3):251-61. doi: 10.1016/s0034-5687(97)02524-3.

DOI:10.1016/s0034-5687(97)02524-3
PMID:9128906
Abstract

This study investigates the effects of autonomic denervation on extravascular lung water, pulmonary hemodynamics, the filtration coefficient of pulmonary vasculature and oxygenation in the development of pulmonary edema. Thirty seven dogs were divided into seven groups. No experimental treatment was conducted in group Nc (n = 4, sham operation) or group Nv (n = 6, bilateral vagotomy) during a 3 h observation period. In the following groups, oleic acid (0.06 ml/kg) was injected into a central vein to induce pulmonary edema: group OAc (n = 6, intact innervation); group OAv (n = 6, bilateral vagotomy); group OAa (n = 6, alpha-blockade by phentolamine); group OAs (n = 6, alpha- and beta-blockade by sympathectomy); and group OAvs (n = 3, vagosympathectomy). The results showed that in the dogs with normal lungs, bilateral vagotomy per se did not cause lung injury during 3 h of observation. However, in oleic acid pulmonary edema, vagotomy significantly deteriorated pulmonary edema by increasing pulmonary intravascular pressures; Alpha- or alpha- and beta- sympathetic inhibition deteriorated pulmonary edema by increasing pulmonary microvascular permeability. The severity of oleic acid-induced pulmonary edema was same in the dogs with vagosympathectomy as in the dogs with intact innervation. These results suggest the inhibition of vagal or sympathetic innervation will aggravate pulmonary edema in the dog.

摘要

本研究调查了自主神经去神经支配对肺水肿形成过程中血管外肺水、肺血流动力学、肺血管滤过系数及氧合的影响。37只犬被分为7组。在3小时观察期内,Nc组(n = 4,假手术)和Nv组(n = 6,双侧迷走神经切断术)未进行实验性处理。在以下各组中,将油酸(0.06 ml/kg)注入中心静脉以诱导肺水肿:OAc组(n = 6,完整神经支配);OAv组(n = 6,双侧迷走神经切断术);OAa组(n = 6,用酚妥拉明进行α阻断);OAs组(n = 6,通过交感神经切除术进行α和β阻断);以及OAvs组(n = 3,迷走交感神经切除术)。结果显示,在肺功能正常的犬中,双侧迷走神经切断术本身在3小时观察期内未引起肺损伤。然而,在油酸诱导的肺水肿中,迷走神经切断术通过增加肺血管内压力显著加重了肺水肿;α或α和β交感神经抑制通过增加肺微血管通透性加重了肺水肿。迷走交感神经切除术的犬中油酸诱导的肺水肿严重程度与完整神经支配的犬相同。这些结果表明,迷走神经或交感神经支配的抑制会加重犬的肺水肿。

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