Parker J D, Landzberg J S, Bittl J A, Mirsky I, Colucci W S
Department of Medicine, Brigham and Women's Hospital, Boston, MA 02115.
Circulation. 1991 Sep;84(3):1040-8. doi: 10.1161/01.cir.84.3.1040.
We tested the hypothesis that beta-adrenergic receptor-stimulated acceleration of left ventricular (LV) isovolumic relaxation (i.e., positive lusitropic response) is attenuated in patients with severe congestive heart failure (CHF) compared with patients without LV dysfunction or CHF.
The beta-adrenergic agonist dobutamine was infused by the intracoronary route in 14 subjects (normal group, six; CHF patients, eight) and by the intravenous route in a second group of 14 subjects (normal group, four; CHF patients, 10). The positive inotropic response to intracoronary or intravenous dobutamine was substantially and significantly reduced in the patients with CHF. LV isovolumic relaxation rate was determined by the methods of Weiss (TL), Mirsky (T1/2), and by a nonlinear regression technique (TNL). LV isovolumic relaxation assessed by all three methods was significantly prolonged in CHF patients compared with normal subjects. Intracoronary and intravenous infusions of dobutamine caused significant acceleration of LV isovolumic relaxation in both normal subjects and patients with CHF. The magnitude of the dobutamine-stimulated acceleration of isovolumic relaxation in patients with CHF was comparable with that in normal subjects.
These data demonstrate that beta-adrenergic receptor stimulation causes significant acceleration of LV isovolumic relaxation in both normal subjects and patients with severe CHF. Coronary to our hypothesis, the lusitropic response to beta-adrenergic stimulation is well preserved in patients with severe CHF despite substantial attenuation of the beta-adrenergic positive inotropic response. These findings have potentially important implications regarding the physiology and pharmacology of adrenergically mediated LV relaxation in humans.
我们检验了这样一个假设，即与无左心室功能障碍或充血性心力衰竭（CHF）的患者相比，严重CHF患者中β-肾上腺素能受体刺激引起的左心室（LV）等容舒张加速（即正性变松弛反应）减弱。
14名受试者（正常组6名；CHF患者8名）通过冠状动脉内途径输注β-肾上腺素能激动剂多巴酚丁胺，另一组14名受试者（正常组4名；CHF患者10名）通过静脉途径输注。CHF患者对冠状动脉内或静脉注射多巴酚丁胺的正性肌力反应显著降低。LV等容舒张率通过Weiss方法（TL）、Mirsky方法（T1/2）以及非线性回归技术（TNL）测定。与正常受试者相比，所有三种方法评估的CHF患者LV等容舒张均显著延长。冠状动脉内和静脉输注多巴酚丁胺在正常受试者和CHF患者中均引起LV等容舒张显著加速。CHF患者中多巴酚丁胺刺激的等容舒张加速幅度与正常受试者相当。
这些数据表明，β-肾上腺素能受体刺激在正常受试者和严重CHF患者中均引起LV等容舒张显著加速。与我们的假设相反，尽管β-肾上腺素能正性肌力反应显著减弱，但严重CHF患者对β-肾上腺素能刺激的变松弛反应仍得到良好保留。这些发现对人类肾上腺素能介导的LV舒张的生理学和药理学具有潜在的重要意义。
