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慢性缺氧时心脏对β-肾上腺素能刺激反应减弱的机制。

Mechanism of the attenuated cardiac response to beta-adrenergic stimulation in chronic hypoxia.

作者信息

Maher J T, Deniiston J C, Wolfe D L, Cymerman A

出版信息

J Appl Physiol Respir Environ Exerc Physiol. 1978 May;44(5):647-51. doi: 10.1152/jappl.1978.44.5.647.

DOI:10.1152/jappl.1978.44.5.647
PMID:649464
Abstract

A blunting of the chronotropic and inotropic responses of the heart to beta-adrenergic stimulation occurs following chronic exposure to hypobaric hypoxia. To pursue the mechanism(s) involved, observations were made in six intact, conscious goats at sea level and in another six goats maintained in a decompression chamber at 445 Torr (approximately 4,300m) for 10 days (Pao2 = 43 Torr). No significant group differences in cardiac frequency and various indices of myocardial performance (peak dP/dt, time-to-peak dP/dt, Vmax) were demonstrable either before or after cholinergic blockade with intravenous atropine methyl bromide, 1 mg/kg. Following hemodynamic studies, thoracotomies were performed and full-thickness biopsies were obtained from the free wall of each of the cardiac chambers. Neither monoamine oxidase activity nor norepinephrine level of any region of the heart was altered by chronic hypoxia. However, a twofold increase (P less than 0.001) in catechol O-methyltransferase activity above sea-level values was found in both the atria and ventricles of the hypoxic animals. Thus, the attenuation in cardiac responsiveness to beta-adrenoceptor stimulation in chronic hypoxia appears unrelated to the level of vagal activity, but may be attributable to enhanced enzymatic inactivation of catecholamines.

摘要

长期暴露于低压低氧环境后,心脏对β-肾上腺素能刺激的变时性和变力性反应会减弱。为探究其中的机制,我们对6只处于海平面的完整清醒山羊以及另外6只在减压舱中于445托(约4300米)环境下维持10天(动脉血氧分压=43托)的山羊进行了观察。静脉注射1毫克/千克甲基溴化阿托品进行胆碱能阻滞前后,两组在心率及心肌性能的各项指标(最大dp/dt、达峰时间、Vmax)上均未显示出显著差异。在进行血流动力学研究后,实施开胸手术并从每个心腔的游离壁获取全层活检组织。慢性低氧并未改变心脏任何区域的单胺氧化酶活性或去甲肾上腺素水平。然而,在低氧动物的心房和心室中,儿茶酚-O-甲基转移酶活性比海平面值增加了两倍(P<0.001)。因此,慢性低氧时心脏对β-肾上腺素能受体刺激反应的减弱似乎与迷走神经活动水平无关,而可能归因于儿茶酚胺的酶促失活增强。

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