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Articles in PresS, published online ahead of print October 24, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00564.2002
Submitted on July 8, 2002
Accepted on October 18, 2002
1 Laboratoire de Pharmacologie, INSERM E 00.01, Faculte de Medecine Paris-Sud, LE KREMLIN-BICETRE, France; Service de Cardiologie, Hopital Antoine Beclere, CLAMART, France
2 Laboratoire de Pharmacologie, INSERM E 00.01, Faculte de Medecine Paris-Sud, LE KREMLIN-BICETRE, France
3 Federation de Cardiologie, Hopital Henri Mondor, CRETEIL, France
* To whom correspondence should be addressed. E-mail: alain.berdeaux{at}kb.u-psud.fr.
The respective contributions of heart rate (HR) reduction and left ventricular (LV) negative inotropy to the effects of antianginal drugs are debated. Accordingly, eight instrumented dogs were investigated during exercise at spontaneous and paced HR (250 beats/min) after administration of either saline, atenolol or ivabradine (selective pacemaker If-channel blocker). During exercise, atenolol and ivabradine (both 1mg/kg, iv) similarly reduced HR (-30% from 222±5 beats/min) and LV mean ejection wall stress was not altered. LV dP/dtmax was reduced by atenolol but not ivabradine. Diastolic time (DT) was increased by atenolol vs saline (195±6 vs 123±4ms, respectively) and to a greater extent by ivabradine (233±11ms). Myocardial oxygen consumption (MVO2) was lower under ivabradine and atenololvs saline (6.7±0.6 and 4.7± 0.4 vs 8.1±0.6ml/min, respectively, p<0.05). Under pacing, DT and MVO2 were similar between ivabradine and saline, but significantly reduced with atenolol. Thus, HR reduction and negative inotropy equally contribute to the reduction in MVO2 during exercise in the normal heart. The negative inotropy limits the increase in DT afforded by HR reduction.
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