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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所致。我们确定了大剂量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）注入在恒压下灌注肝素化血液的离体狗肺中。两种儿茶酚胺都会增加肺毛细血管压力，但会降低肺重量。通过毛细血管滤过系数 (Kfc) 和等重毛细血管压力评估的肺血管通透性在输注儿茶酚胺后 30 和 60 分钟没有显着变化。这些结果表明，大剂量的儿茶酚胺不会增加离体狗肺的肺血管通透性。事实上，肺对肾上腺素的反应与对血小板活化因子 (PAF) 和稳定的血栓素 A_2 类似物 (TxA_2) 的反应形成鲜明对比。在用PAF或TxA_2治疗的肺中，毛细血管压力同样增加至与用肾上腺素治疗的肺相当的水平，但肺重量逐渐增加。这一比较表明，经肾上腺素治疗的肺的肺血管通透性明显小于经PAF或TxA_2治疗的肺，并且可能强化儿茶酚胺不会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部的交感神经的激活是否会导致肺血管通透性增加。通过电刺激星状神经节节后纤维的离体犬或兔肺的 Kfc 评估，未发现肺血管通透性发生变化。这些发现表明交感神经系统可能在肺循环的完整性中不起关键作用。较少的