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目的检测缺氧性肺动脉高压(HPH)大鼠血浆和肺匀浆中尾加压素(U-Ⅱ)、一氧化氮(NO)和C型利钠肽(CNP)的变化,探讨氧疗及这些因子在HPH中的作用。方法雄性W istar大鼠30只均分为对照组、缺氧组、氧疗组。测定各组平均体动脉压(mSAP)、肺动脉平均压(mPAP)、右室肥厚指数(RVH I),血浆U-Ⅱ、NO、CNP水平,肺匀浆U-Ⅱ、CNP水平,光镜观察肺动脉结构改变,扫描电镜观察肺小动脉超微结构。结果缺氧组大鼠mPAP、RVH I[(34.1±2.8)mm Hg、0.43±0.11]显著高于对照组[(18.9±2.0)mm Hg、0.28±0.04,P均<0.01],血浆U-Ⅱ、NO、CNP[(4.4±0.9)pg/m l、(20.8±7.0)μmol/L、(6.6±1.2)pg/m l]均显著高于对照组[(0.9±0.4)pg/m l、(13.2±2.0)μmol/L、(4.0±0.6)pg/m l,P均<0.01],肺匀浆U-Ⅱ、CNP[(6.3±0.5)、(1.89±0.43)pg/m l]亦显著高于对照组[(2.6±0.5)、(0.69±0.21)pg/m l,P均<0.01]。氧疗组大鼠mPAP,血浆U-Ⅱ、NO、CNP,肺匀浆U-Ⅱ、CNP分别为(31.4±2.0)mm Hg,(2.1±0.7)pg/m l、(14.8±1.7)μmol/L、(4.4±0.7)pg/m l,(3.5±0.8)pg/m l、(0.74±0.17)pg/m l;与缺氧组比较差异均有统计学意义(P均<0.01),而RVH I差异无统计学意义(P>0.05)。光镜和电镜下,氧疗组肺血管形态学改变较缺氧组轻。结论缺氧导致HPH形成,U-Ⅱ、NO和CNP参与HPH的病理生理过程,这些因子之间比值失衡可能是导致HPH发生发展的因素之一。
Objective To investigate the changes of urotensin (U-Ⅱ), nitric oxide (NO) and C-type natriuretic peptide (CNP) in plasma and lung homogenate of hypoxic pulmonary hypertension (HPH) The role of factors in HPH. Methods Thirty male Wistar rats were divided into control group, hypoxia group and oxygen therapy group. Mean arterial pressure (mSAP), mean pulmonary artery pressure (mPAP), right ventricular hypertrophy index (RVH I), plasma U-Ⅱ, NO and CNP levels, lung homogenate U- Pulmonary artery structure changes, scanning electron microscopy pulmonary arteriole ultrastructure. Results The levels of mPAP, RVH I [(34.1 ± 2.8) mm Hg, 0.43 ± 0.11] in hypoxic group were significantly higher than those in control group [(18.9 ± 2.0) mm Hg, 0.28 ± 0.04, P <0.01] The levels of NO, CNP [(4.4 ± 0.9) pg / ml, (20.8 ± 7.0) μmol / L and (6.6 ± 1.2) pg / ml] were significantly higher than those in the control group The levels of U-Ⅱ, CNP [(6.3 ± 0.5), (1.89 ± 0.43) pg / ml] in lung homogenate were significantly higher than those in control group (13.2 ± 2.0 μmol / L, 4.0 ± 0.6 pg / ml, P <0.01) In the control group [(2.6 ± 0.5), (0.69 ± 0.21) pg / ml, P <0.01]. (31.4 ± 2.0) mm Hg, (2.1 ± 0.7) pg / ml, (14.8 ± 1.7) μmol / L, (4.4 ± 0.7) pg / ml, (3.5 ± 0.8) pg / ml, and (0.74 ± 0.17) pg / ml respectively. There were significant differences between the two groups (P <0.01) The difference was not statistically significant (P> 0.05). Under light microscope and electron microscope, pulmonary vascular morphological changes in oxygen therapy group were lighter than those in hypoxia group. Conclusions Hypoxia leads to the formation of HPH and the involvement of U-Ⅱ, NO and CNP in the pathophysiology of HPH. The imbalance of these factors may be one of the factors leading to the development of HPH.