中文摘要：

本研究通过肌肉收缩描记方法，应用α1肾上腺素能受体激动剂——苯肾上腺素（Phenylephrine,PE）和α1受体阻断剂——哌唑嗪（prazosin,PRA）探讨慢性间歇性低压低氧（chronic intermittent hypobaric hypoxia, CIHH）大鼠心室乳头状肌α1受体的变化以及α1受体在心脏保护中的作用。雄性Sprague-Dawley大鼠66只，随机分为4组：对照组（control，Con）、CIHH处理14天组（CIHH14）、CIHH处理28天组（CIHH28）和CIHH处理42天组（CIHH42）。CIHH处理动物置于低压氧舱内，分别接受14、28、42天相当于5000m高原（p_B=404mmHg，P_O2=84mmHg）低氧处理，每天6h。对照组动物除不接受低氧处理外，其余条件同CIHH处理动物。大鼠以戊巴比妥钠（3．0-3．5mL／kg体重）腹腔注射麻醉后立即取出心脏，分离右室乳头状肌，用氧饱和的改良台氏液恒温（37℃）、恒速（12mL／min）灌流，电刺激诱发乳头状肌收缩。通过累加给药法，观察不同浓度（1×10^-7、1×10^-6和1×10^-5mol/L）PE对大鼠乳头状肌收缩的影响；用模拟缺血液以及加入PRA（1×10^-6mol／L）的模拟缺血液灌流，观察各组乳头状肌收缩的变化。结果如下：（1）PE增加各组乳头状肌的最大收缩力（maximal isometric tension，P_max）和最大张力上升速率（maximal velocity of tension development, PdT/dt）,作用呈剂量依赖性（P〈0．05）；CIHH28、CIHH42处理组乳头状肌对PE反应性增强（P〈0．05）。最大浓度PE（1×10^-5mol／L）作用下，CIHH28组的P_max和PdT/dt分别较基础值增加51．2％和44．5％，CIHH42组的P_max和PdT/dt分别增加48．6％和44．5％，较对照组（28．7％和24．5％）明显增加（P〈0．05）；（2）CIHH处理可以对抗模拟缺血液对乳头状肌收缩的抑制。CIHH28和CIHH42组的P_max和PdT/dt降低幅度分别为59．6％，53．6％和60．4％，49．9％，明显小于对照组（74．4％，64．7％）（P〈0．05）；?

英文摘要：

The purpose of the present study was to investigate the effect of chronic intermittent hypobaric hypoxia （CIHH） on α1-adrenergic receptors and the role of a1-adrenergic receptors in the protection of CIHH against ischemic injury of myocardium. Sixty-six adult male Sprague-Dawley rats were randomly divided into four groups： control group （Con）, 14-day CIHH treatment group （CIHH14）, 28-day CIHH treatment group （CIHH28） and 42-day CIHH treatment group （CIHH42）. CIHH rats were exposed to hypoxia mimicking 5 000 m altitude （p_B=404 mmHg, p_O2=84 mmHg） in a hypobaric chamber, 6 h daily for 14, 28 and 42 d, respectively. Control animals lived in the same environment as CIHH animals except hypoxia exposure. After anesthesia with sodium pentobarbital （3.0-3.5 mL/kg body weight, i.p.）, papillary muscle was taken from the fight ventricle of rat and perfused with modified Tyrode＇s solution continuously, at constant temperature （37℃） and perfusion speed （12 mL/min）. Muscle contraction was evoked by electric stimuli. Different concentrations （1×10^-7, 1×10^-6 and 1×10^-5 mol/L） of phenylephrine （PE）, an α1-adrenergic receptor agonist, were applied cumulatively to investigate the effect of PE on the mechanic contraction of fight ventficular papillary muscles of rats in Con, CIHH14, CIHH28 and CIHH42 groups. Also, prazosin （1×10^-6 mol/L）, an a1-adrenergic receptor antagonist, was used to investigate the role of α1-adrenergic receptor in the protective effect of CIHH on papillary muscle. The results showed： （1） PE increased the maximal isometric tension （Pmax） and maximal velocity of tension development （PdT/at） of muscle contraction in a dose-dependent manner （P〈 0.05）, and the increase of the muscle contraction was much greater in CIHH28 and CIHH42 rats than that in Con rats （P〈0.05）. Under 1×10^-5 mol/L of PE, the increases of Pmax and PdT/dt over the baseline were 51.2% and 44.5% in CIHH28 group, 48.6% and 44.5% in CIHH42 group, and 28.7%