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[尾加压素II及其受体在肺动脉高压大鼠右心室中的表达]

[Expression of Urotensin II and its receptor on right ventricle in rats of pulmonary hypertension].

作者信息

Huang Hong, Gong Yong-Sheng, Fan Xiao-Fang, Hu Liang-Gang, Luo Jian-Feng, Wu Xiao-Mai

机构信息

Institute of Cor Pulmonale, Wenzhou Medical College, Wenzhou 325027, China.

出版信息

Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2006 Feb;22(1):81-4.

Abstract

AIM

To observe the expression of Urotensin II (U II) and its receptor (UT) on right ventricle in rats with chronic pulmonary hypertension induced by hypoxia and hypercapnia.

METHODS

Twenty male SD rats were randomly divided into normal control group (NC) and hypoxia-hypercapnia 4-week group(HH). Mean pulmonary arterial pressure(MPAP) and the weight ratio of right ventricle (RV) to left ventricle plus septum (LV+ S) were calculated separately. U II in plasma was measured using radioimmunoassay. The expression of U II was observed in right ventricle myocytes and right ventricle arteries by immunohistochemistry. The expression of U II mRNA and UT mRNA were observed in right ventricle myocytes and right ventricle arteries by in situ hybridization.

RESULTS

(1) The MPAP and RV/LV + S of HH group were higher respectively than those of NC group (P < 0.01, respectively). (2) The plasma U II content of HH group did not increased obviously than that of NC group. (3) The expression score of U II, U II mRNA, UT mRNA by right ventricle myocytes in HH group were higher significantly than those of NC group (P < 0.01 respectively). (4) The average value of integral light density (LD) of U II, U II mRNA, UT mRNA by right cardial arteries in HH group were higher significantly than those of NC group (P < 0.01, respectively).

CONCLUSION

The expression of U II in right ventricle arteries and right ventricle myocytes increase significantly during the formation of pulmonary hypertension and right ventricle hypertrophy in rats chronically exposed to hypoxia-hypercapnia. These changes indicate that U II might be involved in right ventricle remodeling, which promotes proliferation of cardiac muscle cells.

摘要

目的

观察尾加压素II(U II)及其受体(UT)在低氧高碳酸血症诱导的慢性肺动脉高压大鼠右心室中的表达。

方法

将20只雄性SD大鼠随机分为正常对照组(NC)和低氧高碳酸血症4周组(HH)。分别计算平均肺动脉压(MPAP)及右心室(RV)与左心室加室间隔(LV+S)的重量比。采用放射免疫分析法测定血浆中的U II。通过免疫组织化学观察右心室心肌细胞和右心室动脉中U II的表达。通过原位杂交观察右心室心肌细胞和右心室动脉中U II mRNA和UT mRNA的表达。

结果

(1)HH组的MPAP和RV/LV + S分别高于NC组(分别为P < 0.01)。(2)HH组血浆U II含量较NC组无明显增加。(3)HH组右心室心肌细胞中U II、U II mRNA、UT mRNA的表达评分显著高于NC组(分别为P < 0.01)。(4)HH组右心室动脉中U II、U II mRNA、UT mRNA的积分光密度(LD)平均值显著高于NC组(分别为P < 0.01)。

结论

在长期暴露于低氧高碳酸血症的大鼠肺动脉高压和右心室肥厚形成过程中,右心室动脉和右心室心肌细胞中U II的表达显著增加。这些变化表明U II可能参与右心室重构,促进心肌细胞增殖。

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