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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发生中的作用。本研究的目的之一是确定神经源性肺水肿的机制，神经源性肺水肿是由大量交感神经激活引起的，并已被证明是由于血管通透性增加。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 μ g）输注到在恒定压力下用肝素化血液灌注的离体狗肺中。这两种儿茶酚胺增加肺毛细血管压力，但减少肺重量。肺血管通透性，毛细血管滤过系数（Kfc）和等重毛细血管压力评估，并没有显着改变，在30和60分钟后输注的任一儿茶酚胺。这些结果表明，大剂量的儿茶酚胺并不增加肺血管通透性在离体狗肺。事实上， ...更多信息对肾上腺素的反应与对血小板活化因子（PAF）和血栓素A_2类似物（TxA_2）的反应相反。PAF或TxA_2处理的肺，毛细血管压力也增加到与肾上腺素处理的肺相当的水平，但肺重量进行性增加。结果表明，肾上腺素处理的肺血管通透性明显小于PAF或TxA_2处理的肺血管通透性，从而进一步证实了儿茶酚胺不增加肺微血管通透性的结论。本研究的另一个主要目的是确定支配肺的交感神经的激活是否引起肺血管通透性的增加。肺血管通透性的KFC评价无论是离体犬或兔肺，其节后纤维的星状神经节电刺激没有发现变化。提示交感神经系统对肺循环的完整性可能不起决定性作用。少