吸入一氧化氮降低烟雾吸入性损伤肺动脉高压的实验研究

烟雾吸入致肺组织细胞损伤后５ｍｉｎ，行肺灌洗机械通气４ｈ，观察２４。酹明，犬随机分为三组。烟雾吸入后，对照组单纯涓氧；治疗组吸氧加０．００４５％ＮＯ，连续监测１２ｈ血循环动力学化；正常组不致伤。

An experiment study of reversed pulmonary hypertension with inhaled nitric oxide on smoke inhalation injury]

We evaluated the effect and mechanisms of reversed pulmonary hypertension with inhaled nitric oxide (NO) on smoke inhalation injury in the dog model, 21 dogs were divided into 3 groups randomly. Following smoke inhalation, the control group (n = 8) inhaled O2 (FiO2, 0.45) and the treated group (n = 9) inhaled O2 and 0.0045% (45 ppm) NO. Hemodynamics was serially measured for 12 hours. In addition, 4 dogs without smoke inhalation were used to study the normal lung histomophologic findings. The data were analyzed by ANOVA. After inhalation of NO, the mean pulmonary artery pressure (mPAP), pulmonary minute vessels pressure (Pmv), and pulmonary vascular resistance (PVR) were decreased significantly (P < 0.05), while the mean aortic pressure (mAP) and total peripheral resistance (TRP) were not remarkably changed (P > 0.05). The levels of cyclic guanosine monophosphate (cGMP) were increased significantly (P < 0.01). Inhaled NO may reverse pulmonary hypertension with smoke inhalation injury in dogs. The mechanism of selective pulmonary circulation was increased cGMP level in smooth cells. Inhaled NO may be recommended for clinical application.