The role of sympathetic nervous system in the genesis of pulmonary edema

交感神经系统在肺水肿发生中的作用

基本信息

批准号：
05454420
负责人：
SHIBAMOTO Toshishige
金额：
$ 4.1万
依托单位：
Shinshu University School of Medicine
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (B)
财政年份：
1993
资助国家：
日本
起止时间：
1993 至 1995
项目状态：
已结题

项目摘要

We studied the role of sympathetic nervous system in the genesis of pulmonary edema. One of the purpose of this study was to determine the mechanism for neurogenic pulmonary edema, which is caused by massive sympathetic activation and has been demonstrated to be due to increased vascular permeability. We determined the effects of large doses of catecholamines on pulmonary vascular permeability. Epinephrine or norepinephrine (100,300 mug) was infused into isolated dog lungs perfused with heparinized blood at constant pressure. Both catecholamines increased the pulmonary capillary pressure but reduced the lung weights. The pulmonary vascular permeability, assessed by the capillary filtration coefficient (Kfc) and the isogravimetric capillary pressure, did not change significantly at 30 and 60 min after infusion of either catecholamine. These results suggest that large doses of catecholamines do not increase the pulmonary vascular permeability in isolated dog lungs. Indeed, the lung weigh … More t response to adrenaline contrasted with the responses to platelet-activating factor (PAF) and the stable thromboxane A_2 analogue (TxA_2). In lungs treated with PAF or TxA_2, capillary pressure similarly increased to the level equivalent to that in the adrenaline-treated lungs, but lung weight progressively increased. This comparison indicates that pulmonary vascular permeability of adrenaline-treated lungs is apparently smaller than that of lungs treated with either PAF or TxA_2, and may reinforce the conclusion that catecholamines do not increase pulmonary microvascular permeability. Another major purpose of this study was to determine whether activation of sympathetic nerve innervating lung causes an increase in pulmonary vascular permeability. No changes were found in pulmonary vascular permeability as evaluated by Kfc of either isolated canine or rabbit lungs, whose postganglionic fibers of stellate ganglions were electrically stimulated. These findings suggest that sympathetic nervous system may not play a crucial role in the integrity of pulmonary circulation. Less

我们研究了交感神经系统在肺水肿起源中的作用。这项研究的目的之一是确定神经源性肺水肿的机制，该机制是由大量交感神经激活引起的，已证明是由于血管通透性增加所致。我们确定了大剂量的儿茶酚胺对肺血管通透性的影响。将肾上腺素或去甲肾上腺素（100,300杯）注入孤立的狗肺中，在恒定压力下用肝素化的血液灌注。两种儿茶酚胺都会增加肺毛细管压力，但减少了肺部的重量。通过毛细管过滤系数（KFC）评估的肺血管通透性和等值毛毛细管压力在输注两Catecholamine后30和60分钟时没有显着变化。这些结果表明，大剂量的儿茶酚胺不会增加分离的狗肺的肺血管通透性。实际上，肺重量……对肾上腺素的更多反应与对血小板激活因子（PAF）和稳定的血栓烷A_2模拟（TXA_2）的反应形成对比。在用PAF或TXA_2处理的肺中，毛细管压力与相当于肾上腺素治疗的肺部的水平相似，但肺部体重逐渐增加。该比较表明，肾上腺素治疗的肺的肺血管通透性显然小于用PAF或TXA_2处理的肺部的肺部渗透性，并且可能会加强结论，即儿茶酚胺不会增加肺部微血管渗透性。这项研究的另一个主要目的是确定交感神经支配肺的激活是否会导致肺血管通透性的增加。通过肯德基评估了孤立的犬或兔肺的肺血管渗透性，在肺血管通透性中没有变化，其恒星神经节的后神经节纤维受到电刺激。这些发现表明，交感神经系统在肺循环的完整性中可能不起作用。较少的