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目的探讨长期雾化吸入硝酸甘油对高肺血流大鼠肺动脉压力、肺血管结构的作用及其机制。方法24只健康雄性Wistar大鼠随机分为对照组、分流组和吸入组。对分流组和吸入组大鼠开腹行腹主动脉-下腔静脉分流术,12周后两组大鼠分别雾化吸入生理盐水和硝酸甘油3周。以右心导管法测定肺动脉压,颈动脉插管测定体循环压,检测右心室肥厚,观测肺血管显微及超微结构变化,用免疫组织化学法检测大鼠肺动脉人类尾加压素Ⅱ(hUⅡ)的表达。结果分流组大鼠肺动脉平均压(PAMP)和右心室/左心室+室间隔重量比值(RV/LV+S)明显高于对照组(P<0.01),且分流组大鼠肺小血管肌化程度明显增强(P<0.01),中、小型肺肌型动脉相对厚度(RMT)增加,肺动脉内皮细胞和平滑肌细胞hUⅡ表达明显增强。吸入组大鼠mSBP未受影响,PAMP明显低于分流组(P<0.01),RV/(LV+S)高于对照组(P<0.01),但与分流组比较差异无显著性(P>0.01),吸入组大鼠肺小血管肌化程度明显改善,小型肺肌型动脉RMT及小型肺动脉内皮细胞和平滑肌细胞hUⅡ减少。结论长期雾化吸入硝酸甘油可缓解高肺血流量所致肺动脉高压和肺血管结构的重建,其对肺动脉内皮细胞和平滑肌细胞hUⅡ表达的抑制作用,可能参与高肺血流量所致肺血管结构重建和肺动脉高压的调节。
Objective To investigate the effect of long-term inhalation of nitroglycerin on pulmonary artery pressure and pulmonary vascular structure in rats with high pulmonary blood flow and its mechanism. Methods Twenty-four healthy male Wistar rats were randomly divided into control group, shunt group and inhalation group. Paracentesis and inferior vena cava bypass were performed in shunt group and inhalation group. After 12 weeks, rats in both groups were inhaled with normal saline and nitroglycerin respectively for 3 weeks. Pulmonary arterial pressure was measured by right heart catheterization, systemic pressure was measured by carotid artery cannulation, right ventricular hypertrophy was measured, microscopic and ultrastructural changes of pulmonary vessels were observed. Immunohistochemistry was used to detect the expression of human urotensin Ⅱ (hUⅡ )expression. Results The pulmonary artery mean pressure (PAMP) and RV / LV + S ratio in the shunt group were significantly higher than those in the control group (P <0.01) (P <0.01). The relative thickness of middle and small pulmonary arteries increased (RMT), and the expression of hUⅡ in pulmonary artery endothelial cells and smooth muscle cells increased significantly. The inhaled mSBP was not affected, the PAMP was significantly lower than the shunt group (P <0.01), RV / (LV + S) was higher than the control group (P <0.01), but there was no significant difference compared with the shunt group 0.01). The pulmonary vascular remodeling was significantly improved in inhaled rats, and the hUⅡ in small pulmonary arterioles and small pulmonary arterial endothelial cells and smooth muscle cells were decreased. Conclusion Long-term inhalation of nitroglycerin can alleviate the pulmonary hypertension and pulmonary vascular remodeling induced by high pulmonary blood flow, which can inhibit the expression of hUⅡ in pulmonary artery endothelial cells and smooth muscle cells, and may be involved in pulmonary vascular remodeling caused by high pulmonary blood flow And pulmonary hypertension.