吸入一氧化氮降低吸入性损伤所致肺动脉高压的实验研究

The effect and mechanisms of reversed pulmonary hypertension with Inhaled nitric oxide on smoke inhalation injury in dogs

为评价吸入一氧化氮(NO)在犬烟雾吸入性损伤的降压效果及验证其作用机制。将21只犬随机分为三组,烟雾吸入后,对照组(n=8),单纯吸氧(FiO_2,0.45),治疗组(n=9)吸氧(FiO_2,0.45)+0.0045％(45ppm)NO,连续监测12h血循环动力学变化;正常组(n=4)不致伤,用于建立组织学对照。结果:吸入NO组平均肺动脉压(mPAP)、肺血管阻力(PVR)明显下降(P<0.05),而平均主动脉压(mAP)、周围血管阻力(TPR)无明显影响(P>0.05)。动脉血和肺组织环磷酸乌苷(cGMP)明显升高(P<0.01)。表明吸入NO可降低吸入性损伤肺动脉高压,选择性作用于肺循环的机理为提高平滑肌细胞内cGMP水平。

21 dogs were divided into 3 groups randomly. Following smoke inhalation, the central group (n=8). inhaled O2(FiO2,0.45) and the treated group (n = 9) .inhaled o2 and 0. 0045% (45ppm) NO,Hemo-dynamics were serially measured for 12 hours; In addition, 4 dogs without smoke inhalaition were used to study the normal lung histomorphologic findings. The data were analyzed by variance (ANOVA). Results, After inhaled NO, mean pulmonary arterial pressure (mPAP) and pulmonary vascular resistance (PVR) were decreased significantly(P<0. 05), While mean Arterial pressure (mAP) and total peripheral resistance (TPR) were not marked changed (P>0. 05). The levels of cyclic guanosine monophosphate (cGMP) were increased significantly (P<0.01). Conclusions,Inhaled NO may reverse pulmonary pertension with inhalation injury. The mechanisms of selective pulmonary circulation were increased of cGMP level in smooth cells.