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机构地区:[1]西藏军区总医院高山病研究中心,拉萨850003 [2]第三军医大学高山病研究所,重庆630038
出 处:《中国应用生理学杂志》1992年第4期294-298,共5页Chinese Journal of Applied Physiology
摘 要:为了探讨α_1、β肾上腺素能受体在大鼠缺氧性心脏肥大进程中的作用,本研究应用放射配基结合法观察了不同缺氧时间大鼠心室α_1、β肾上腺素能受体变化的动态过程,同时也观察了α_1、β受体阻断剂在预防缺氧性心肌肥大发生中的作用。缺氧10d后,测定右心室重量及组织学检查未见右心室肥大,但此时心室肌α_1受体数量从对照组的27.49±1.25增加到33.80±0.90fmol/mg蛋白(P<0.05);β受体从对照组的51.80±7.60下降到25.10±2.30fmol/mg蛋白(P<0.01)。缺氧20和30d后α_1受体进一步增加到40.70±1.43和32.30±1.96fmol/mg蛋白(P<0.05);β受体分别为27.90±2.30和42.80±1.70fmol/mg蛋白(P<0.05)。缺氧20和30d后右心室重量指数明显高于对照组,在整个缺氧过程中α_1、β受体的亲和性(K_d)未见明显变化,未见左心室肥大。缺氧同时应用α_1受体阻断剂(哌唑嗪4mg·kg^(-1)·d^(-1))30d,可明显预防缺氧所致的右心肥大;而β受体阻断剂(心得安10mg·kg^(-1)·d^(-1))没有此种作用。由此可见,在缺氧所致右心肥大之前,心肌α_1受体数量即明显升高,α_1受体阻断剂可以预防缺氧引起的右心肥大。To elucidate the role of α1- and β-adrenergic activities in cardiac hypertrophy during hypoxia, changes of α1- and β-adrenoceptors were examined by radioligand binding assay and the preventive effects of α1- and β-adrenoceptor blockade on cardiac hypertrophy were assessed in rats during hypoxia.After 10 days hypoxia, right ventricular hypertrophy was not found by histological examination. In this period, The Bmax of the ventricular α1-adrenoceptor increased from 27.49 ±1.25 (control) to 33..801 0.90 fmol/mg protein (P<0.05), whereas the Bmax of β-adrenoceptor decreased from 51.80± 7.60 (control) to 25.10±2.30 fmol/mg (hypoxia) (P<0.01). After hypoxia for 20 and 30 days, the Bmax of ventricular α1-adrenoceptor increased further to 40.70 ±1.43 and 32.30 ± 1.96 (P<0.05), while the Bmax of β-adrenoceptor was 27.90 ± 2.30 and 42.80 ± 1.70 fmol / mg protein (P < 0.05) respectively, accompanied by a significant right ventricular hypertrophy. There was no change in Kd of α1,β-adrenoceptors and no left ventricular hypertrophy was found. Simultaneous administration of the α1-blocker prazosin (4mg ·kg-1 · d-1) and hypoxia significantly attenuated the right ventricular hypertrophy, whereas the β-blocker propranolol (10mg· kg-1 ·d-1) did not after hypoxia for 30 days.These results showed that hypoxia elicited an increase in myocardial α1-adrenoceptors before the onset of cardiac hypertrophy, and that an α1-blocker could prevent the development of hypertrophy while an β-blocker could not during hypoxia.
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