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

神经源性肺水肿(NPE)的病理生理学机制，即静水机制和通透性机制，一直存在争议。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的研究进一步复杂化。采用两种体外循环系统，分离肺循环和体循环，建立犬在体肺循环模型。在有或不有心肺神经(CPN)的情况下进行原位肺灌流。首先做了右心搭桥的准备。然后切换到肺灌流准备，肺通过CPN接受大脑和全身循环突然停止的所有影响。通过将肺动脉压力调整到24 mm Hg以下，排除了引起肺水肿的流体静力学机制。CPN切断组的血管外肺水蓄积和再灌注期失血率明显低于CNP完整组。结果就是。提示CPN介导的通透性水肿机制。观察麻醉深度和迷走神经干预对大鼠纤维蛋白诱发NPE的影响。枕大池内注入纤维蛋白原和凝血酶溶液。大鼠以25或50 mg/kg的戊巴比妥钠腹腔注射麻醉。迷走神经干预包括静脉注射阿托品1 mg/kg或双侧迷走神经切断术。计算肺水比为湿肺和干肺重量之差与干肺重量之比。与浅麻醉相比，深麻醉下肺水肿发生率和肺水比例明显降低。轻度麻醉下迷走神经切断组大鼠肺水比明显高于其他组。结果表明，麻醉深度和迷走神经对NPE的发生有影响。

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.