Martinsson A, Melcher A, Lindvall K, Hjemdahl P
Department of Pharmacology, Karolinska Institutet, Stockholm, Sweden.
Acta Physiol Scand. 1991 Feb;141(2):167-80. doi: 10.1111/j.1748-1716.1991.tb09065.x.
The present study was performed to characterize cardiovascular responses to isoprenaline and the influence of autonomic reflexes on these responses. Nine healthy volunteers received infusions and bolus injections of isoprenaline before and after 'autonomic blockade' produced by intravenous atropine 0.04 mg kg-1 and clonidine 300 micrograms. Heart rate, blood pressures, systolic time intervals and various echocardiographic measures of cardiac contractility were registered. No significant differences in responsiveness to isoprenaline were seen when infusions were repeated on the same day without 'autonomic blockade'. After 'blockade', delta responses at 1 nmol l-1 isoprenaline (infusions) were increased for diastolic blood pressure and decreased for systolic blood pressure and stroke volume. Bolus injections of 2 micrograms isoprenaline caused enhanced delta responses after 'autonomic blockade' of diastolic blood pressure, left ventricular diameter in systole, ventricular circumferential fibre shortening, mean posterior wall velocity (Vmean PW), stroke volume, systemic vascular resistance, electromechanical systole (QS2) and pre-ejection period. Systolic blood pressure decreased, in contrast to a small increase without 'blockade'. These findings are explained by differences in haemodynamic effects of isoprenaline and by the dependence of responses on reflexes when isoprenaline is administered in different ways. When heart rate was increased by bolus doses of atropine, in the presence of beta-blockade (propranolol), pre-ejection period and left ventricular diameter in systole were unaffected, and Vmean PW and ventricular circumferential fibre shortening showed only small increases (compared with alterations induced by isoprenaline). However, left ventricular ejection time, QS2 and ejection time (by echocardiography), were markedly dependent on heart rate alterations. Thus, pre-ejection period, left ventricular diameter in systole Vmean PW and ventricular circumferential fibre shortening are parameters which can be useful in order to evaluate cardiac beta-adrenoceptor sensitivity in vivo in man.
本研究旨在描述对异丙肾上腺素的心血管反应以及自主反射对这些反应的影响。9名健康志愿者在静脉注射0.04mg/kg阿托品和300μg可乐定产生“自主神经阻滞”前后,接受了异丙肾上腺素的输注和推注。记录心率、血压、收缩期时间间期以及各种心脏收缩性的超声心动图测量值。在同一天未进行“自主神经阻滞”重复输注时,对异丙肾上腺素的反应性未见显著差异。“阻滞”后,1nmol/L异丙肾上腺素(输注)时舒张压的增量反应增加,收缩压和每搏量的增量反应降低。推注2μg异丙肾上腺素导致“自主神经阻滞”后舒张压、收缩期左心室直径、心室圆周纤维缩短、后壁平均速度(Vmean PW)、每搏量、全身血管阻力、机电收缩期(QS2)和射血前期的增量反应增强。与未“阻滞”时的小幅增加相反,收缩压降低。这些发现可通过异丙肾上腺素的血流动力学效应差异以及以不同方式给予异丙肾上腺素时反应对反射的依赖性来解释。当在存在β受体阻滞剂(普萘洛尔)的情况下通过推注剂量的阿托品使心率增加时,射血前期和收缩期左心室直径未受影响,Vmean PW和心室圆周纤维缩短仅显示小幅增加(与异丙肾上腺素引起的变化相比)。然而,左心室射血时间、QS2和射血时间(通过超声心动图)明显依赖于心率变化。因此,射血前期、收缩期左心室直径、Vmean PW和心室圆周纤维缩短是有助于评估人体体内心脏β肾上腺素能受体敏感性的参数。