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Mechanism and the Effects of Anesthetics and Anesthetic Depth on the Development of Neurogenic Pulmonary Edema.

麻醉药和麻醉深度对神经源性肺水肿发生的机制和影响。

基本信息

批准号：
61480332
负责人：
SHIMADA Yasuhiro
金额：
$ 4.35万
依托单位：
Nagoya 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：
1986
资助国家：
日本
起止时间：
1986 至 1988
项目状态：
已结题

项目摘要

There is a controversy on the pathophysiology of neurogenic pulmonary edema (NPE), namely hydrostatic and permeability mechanisms. When ischemia develops in the central nervous system, hemodynamic changes occur both in systemic and pulmonary circulation, which would further complicate the study on NPE. The authors devoloped canine in situ model using two extracorporeal circulation systems and separating pulmonary circulation from systemic circulation. In situ lungs were perfused in the presence or absence of the cardiopulmonary nerves (CPN). A right-heart bypassed preparation was made first. It was then switched to a lung perfusion preparation and the lungs received all influences of sudden cessation of the brain and systemic circulation via the CPN. Hydrostatic mechanisms causing pulmonary edema were excluded by adjusting the pulmonary arterial preaaure less than 24mmHg. Accumulation of the extravascular lung water and rate of reaervoir blood loss were significantly lower in the CPN-severed group compared to the CNP-intact group. The result. indicates a CPN-mediated mechanism of permeability edema. Effects of the depth of anesthesia and intervention in the vagus nerves on the development of fibrin-induced NPE were examined in rats. Solutions of fibrinogen and thrombin were injected into the cisterna magna. Rats were anesthetized with an intraperitoneal injection of sodium pentobarbital, either 25 or 50mg/kg. Intervention in the vagus nerves consisted of intravenous atropine 1mg/kg or bilateral vagotomy. Lung water ratio was calculated as a ratio of the difference between wet and dry lung weight to dry lung weight. Incidence of pulmonary edema and lung water ratio were significantly decreased under deep anesthesia compared to light anesthesia. Lung water ratio was significantly increased in the vagotomized rats under light anesthesia compared to other groups. The results indicate the effects of anesthetic depth and vagus nerve on the development of NPE.

神经源性肺水肿（NPE）的病理生理机制，即流体静力学机制和通透性机制存在争议。当中枢神经系统发生缺血时，体循环和肺循环都会发生血流动力学变化，这将使NPE的研究更加复杂。作者采用两套体外循环系统，将体循环和肺循环分离，建立了犬在体循环模型。在心肺神经（CPN）存在或不存在的情况下进行原位肺灌注。首先进行右心旁路准备。然后转换为肺灌注准备，肺通过CPN接受脑和体循环突然停止的所有影响。通过调整肺动脉压力小于24 mmHg排除引起肺水肿的流体静力学机制。与CNP完整组相比，切断CPN组的血管外肺水积聚和再灌注失血率显著降低。结果。表明CPN介导的渗透性水肿机制。麻醉深度和迷走神经的干预对纤维蛋白诱导的NPE的发展的影响进行了检查。将纤维蛋白原和凝血酶溶液注入枕大池。大鼠腹腔注射戊巴比妥钠（25或50 mg/kg）麻醉。迷走神经的干预包括静脉注射阿托品1 mg/kg或双侧迷走神经切断术。肺水比计算为湿肺重量和干肺重量之间的差与干肺重量的比率。与浅麻醉相比，深麻醉下肺水肿的发生率和肺水比率显著降低。与其他组相比，在轻度麻醉下切断迷走神经的大鼠肺水比率显著增加。结果表明麻醉深度和迷走神经对NPE的发生有影响。