[尾加压素II、一氧化氮及C型利钠肽在大鼠低氧性肺动脉高压中的表达及意义]

[The expression and significance of urotensin II, nitric oxide, and C-type natriuretic peptide in hypoxia-induced pulmonary hypertension in rats].

作者信息

Sun De-jun, Yang Jing-ping, Sun Yan-hong

机构信息

Department of Respiratory and Critical Medicine, Third Affiliated Hospital of Inner Mongolia Medical College, Baotou 014010, China.

出版信息

Zhonghua Jie He He Hu Xi Za Zhi. 2006 Mar;29(3):185-8.

PMID:16677483

Abstract

OBJECTIVE

To investigate the alteration of plasma and lung tissue homogenate urotensin II (U-II), nitric oxide (NO) and C-type natriuretic peptide (CNP) levels in rats with hypoxia-induced pulmonary hypertension (HPH) and to study the role of these factors and oxygen treatment in the development of HPH.

METHODS

Thirty male Wistar rats were randomly divided into three groups: a control group, a group with hypoxia for 14 days and a group with oxygen treatment after hypoxia for 14 days, 10 rats per group. Mean pulmonary arterial pressure (mPAP), mean systematic arterial pressure (mSAP) and right ventriculo hypertrophy index (RVHI) were measured. The plasma levels of U-II, NO, CNP, and the lung tissue homogenate levels of U-II and CNP were measured. The structure of the pulmonary arteries was examined using optical microscope. The microstructure and ultrastructure changes in pulmonary small arteries were examined using electron microscope.

RESULTS

The mPAP and RVHI in the hypoxia group [(34.1 +/- 2.8) mm Hg, 0.43 +/- 0.11] were higher than those in the control group [(18.9 +/- 2.0) mm Hg, 0.28 +/- 0.04, all P < 0.01]. The plasma levels of U-II, NO, and CNP [(4.4 +/- 0.9) pg/ml, (20.8 +/- 7.0) micromol/L, (6.6 +/- 1.2) pg/ml], and the lung tissue homogenate levels of U-II and CNP [(6.3 +/- 0.5), (1.89 +/- 0.43) pg/ml] in the hypoxia group were higher than those in the control group [(0.9 +/- 0.4) pg/ml, (13.2 +/- 2.0) micromol/L, (4.0 +/- 0.6) pg/ml, (2.6 +/- 0.5) pg/ml, (0.69 +/- 0.21) pg/ml, respectively, all P < 0.01]. Compared with the hypoxia group, the mPAP, the plasma levels of U-II, NO, and CNP, and the lung tissue homogenate levels of U-II and CNP in the oxygen treatment group [(31.4 +/- 2.0) mm Hg, (2.1 +/- 0.7) pg/ml, (14.8 +/- 1.7) micromol/L, (4.4 +/- 0.7) pg/ml; (3.5 +/- 0.8) pg/ml, (0.74 +/- 0.17) pg/ml, respectively] were significantly decreased (all P < 0.01). The pulmonary vessel morphology changes of the oxygen treatment group were ameliorated.

CONCLUSIONS

U-II, NO and CNP are involved in the pathophysiologic process of HPH. Imbalance of these factors may be partially responsible for the development of the disease.

摘要

目的

探讨低氧性肺动脉高压（HPH）大鼠血浆及肺组织匀浆中尾加压素Ⅱ（U-II）、一氧化氮（NO）和C型利钠肽（CNP）水平的变化，研究这些因子及氧疗在HPH发生发展中的作用。

方法

将30只雄性Wistar大鼠随机分为三组：对照组、低氧14天组、低氧14天后氧疗组，每组10只。测定平均肺动脉压（mPAP）、平均体动脉压（mSAP）及右心室肥厚指数（RVHI）。检测血浆U-II、NO、CNP水平及肺组织匀浆U-II和CNP水平。用光镜观察肺动脉结构。用电子显微镜观察肺小动脉的微观和超微结构变化。

结果

低氧组的mPAP和RVHI[（34.1±2.8）mmHg，0.43±0.11]高于对照组[（18.9±2.0）mmHg，0.28±0.04，P均<0.01]。低氧组血浆U-II、NO、CNP水平[（4.4±0.9）pg/ml，（20.8±7.0）μmol/L，（6.6±1.2）pg/ml]及肺组织匀浆U-II和CNP水平[（6.3±0.5），（1.89±0.43）pg/ml]高于对照组[分别为（0.9±0.4）pg/ml，（13.2±2.0）μmol/L，（4.0±0.6）pg/ml，（2.6±0.5）pg/ml，（0.69±0.21）pg/ml，P均<0.01]。与低氧组比较，氧疗组的mPAP、血浆U-II、NO、CNP水平及肺组织匀浆U-II和CNP水平[（31.4±2.0）mmHg，（2.1±0.7）pg/ml，（14.8±1.7）μmol/L，（4.4±0.7）pg/ml；（3.5±0.8）pg/ml，（0.74±0.17）pg/ml]均显著降低（P均<0.01）。氧疗组肺血管形态改变有所改善。