摘要
本文观察常压缺氧性肺动脉高压大鼠肺组织β和β＿２受体以及β受体ｍＲＮＡ含量的变化。动物分对照组，缺氧２周及４周组。用放射性配基结合法测定β和β＿２受体，用反转录一聚合酶链反应（ＲＴ－ＰＣＲ）和液体闪烁计数测定β＿２受体ｍＲＮＡ的变化。结果表明，缺氧２及４周大鼠肺组织β受体从对照组的２２４．９±２３．７ｆｍｏｌ／ｍｇ蛋白分别下降到１４７．０±１９．４和１４２．７±３．１ｆｍｏｌ／ｍｇ蛋白，（均Ｐ＜０．００１）。β＿２受体从对照组的１７３．８±２１．４ｆｍｏｌ／ｍｇ蛋白分别降至６７，１±１１．８和３８．１±４．０ｆｍｏｌ／ｍｇ蛋白，（与对照比及缺氧组间比均Ｐ＜０．００１）。缺氧２周时β＿２受体ｍＲＮＡ水平与对照相比无变化，缺氧４周时明显下降（为对照的４２％，Ｐ＜０．００１）。缺氧４周β＿２受体下降可能与此有关。揭示缺氧后肺β＿２受体下降的分子生物学基础。对肺动脉高压发生发展机制提供新的认识。
Rats were kept in isobaric hypoxic chamber(O_2=10±0.5%)for 2 and4 weeks(6hrs/day,6days/wk ),the subtype of beta-adrenoceptors of lung were measuredby binding technique,RT-PCR ( Reverse-Transcription-Polymerase Chain Reaction )wascombined with LSC(Liquid Scintillation Counting)technique to analyse the expressionof mRNA of beta 2-adrenoceptors.The results showed that the lung beta and beta 2-adrenoceptor decreased significantly after 2 and 4 weeks hypoxia. The lung beta 2-adre-noceptor decreased from 173.8 ± 21.4 fmol/mg protein to 67.1±11.8 and 38.1± 4.0fmol/mg protein (all P<0.001)after 2 and 4 wks hypoxia. It was also found that theexpression of beta 2-adrenoceptor mRNA decreased significantly after 4 weeks hypoxia(only 42%of control leve1,P<0.001). But no change was found after 2 weeks hypoxia.The data indicated the reduced density of beta 2-adrenoceptor might play role in thedevelopment of hypoxic pulmonary hypertension.The reduction of beta 2-adrenoceptorafter 4 weeks hypoxia was related to the decrease of deta 2-adrenoceptor mRNA.Thisfinding might shed a new light on the understanding pathogenesis of pulmonary hyper-tension.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
1995年第1期6-10,共5页
Chinese Journal of Pathophysiology
基金
"八五"国家攻关课题
