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作 者:黄虹[1] 龚永生[1] 范小芳[1] 胡良冈[1] 骆健峰[1] 吴小脉[1]
机构地区:[1]温州医学院肺心病研究室
出 处:《中国应用生理学杂志》2006年第1期81-84,i0005,共5页Chinese Journal of Applied Physiology
基 金:浙江省教委科研基金资助项目(20020468);温州市科委基金资助项目(Y2003A037)
摘 要:目的:观察尾加压素Ⅱ(UⅡ)及其受体UT在慢性低O2高CO2肺动脉高压大鼠右心室的表达。方法:健康SD大鼠20只随机分成正常对照组和低氧高二氧化碳4周(HH)组,分别测定平均肺动脉压力(mPAP),右心室游离壁(RV)和左心室加室间隔(LV+S)的重量比;放免法测定大鼠血浆UⅡ含量;免疫组化方法检测心肌细胞、心肌小动脉UⅡ蛋白的表达;组织原位杂交方法检测心肌细胞、心肌小动脉UⅡmRNA和UⅡ受体(UT)mRNA的表达。结果:①HH组mPAP和RV/LV+S比正常对照组分别高52.0%与25.4%(P均<0.01)。②HH组血浆UⅡ水平较正常对照组无明显增高。③免疫组化显示HH组心肌细胞UⅡ蛋白表达阳性率和心肌小动脉UⅡ蛋白表达的平均吸光度值均明显高于正常对照组(P<0.01)。④组织原位杂交可见HH组的心肌细胞UⅡmRNA表达阳性率和心肌小动脉UⅡmRNA表达的平均吸光度值均明显高于正常对照组(P均<0.01)。⑤组织原位杂交可见HH组的心肌细胞UT mRNA表达阳性率和心肌小动脉UT mRNA表达的平均吸光度值均较正常对照组明显增高(P均<0.01)。结论:慢性低氧高二氧化碳性大鼠肺动脉高压及右室肥大形成过程中,心肌小动脉和心肌细胞的UⅡ及其受体UT的表达均呈现明显上调,提示UⅡ可能有促进心肌细胞增殖,导致右心室重构的作用。推测UⅡ在慢性低氧高二氧化碳性肺动脉高压及右室肥大的形成机制中具有重要的病理生理意义。Aim: To observe the expression of Urotensin Ⅱ(U I1 ) 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 UⅡ was observed in right ventricle myocytes and right ventricle arteries by immunohistochemistry. The expression of UⅡ 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). ②The plasma UⅡ content of HH group did not increased obviously than that of NC group, ③The expression score of UⅡ ,U Ⅱ mRNA, UT mRNA by right ventricle myocytes in HH group were higher significantly than those of NC group( P 〈 0.01 respectively). ④The average value of integral light density(LD) of UⅡ , UⅡ 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 UⅡ 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 UⅡ might be involved in right ventricle remodeling, which promotes prolifera- tion of cardiac muscle cells.
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