论文部分内容阅读
目的:探讨波生坦对高原性肺动脉高压的治疗作用及其对NO的影响。方法:SD大鼠随机分为:正常组,安慰剂组和波生坦。除正常组外,其他组置于减压中,8 h/d,持续6周。自第4周起,安慰剂组和波生坦组的大鼠在低压低氧前分别给与生理盐水或波生坦灌胃。测定各组大鼠的平均肺动压(mPAP)、右心室肥厚指数(RV/LV+S%)、肺系数;测定各组大鼠动脉血和肺组织中NO的含量以及肺组织中NOS的活性。结果:和正常组相比,安慰剂组大鼠的mPAP,RV/LV+S%和肺系数显著升高;波生坦能显著抑制RV/LV+S%和肺系数的升高,并使mPAP下降至正常组水平。安慰剂组大鼠动脉血及肺组织中NO的含量和肺组织中NOS的活性都明显降低于正常组;波生坦治疗组大鼠动脉血和肺组织中NO的含量以及肺组织中NOS的活性较安慰剂组都显著升高。结论:波生坦通过增加低压低氧大鼠体内NOS的活性和NO的含量,来发挥其治疗高原性肺水肿的作用。
Objective: To investigate the therapeutic effect of bosentan on high altitude pulmonary hypertension and its effect on NO. Methods: SD rats were randomly divided into normal group, placebo group and bosentan. In addition to the normal group, other groups were placed in decompression, 8 h / d, for 6 weeks. From Week 4, rats in the placebo and bosentan groups were given gavage with physiological saline or bosentan respectively before hypobaric hypoxia. The mean pulmonary arterial pressure (mPAP), right ventricular hypertrophy index (RV / LV + S%) and pulmonary coefficient of rats in each group were measured. The content of NO in arterial blood and lung tissue and the content of NOS active. Results: Compared with the normal group, mPAP, RV / LV + S% and pulmonary coefficient of the placebo group were significantly increased; bosentan significantly inhibited RV / LV + S% and pulmonary coefficient, mPAP decreased to normal group level. The NO content in the arterial blood and lung tissue and the activity of NOS in the lung tissue in the placebo group were significantly lower than those in the normal group. The NO content in the arterial blood and lung tissue in the bosentan-treated group and the NOS in the lung tissue Activity than the placebo group were significantly higher. CONCLUSION: Bosentan exerts its therapeutic effect on high altitude pulmonary edema by increasing the activity of NOS and the content of NO in hypoxic hypoxia rats.