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OtherCARDIOVASCULAR PHARMACOLOGY

The Cardiac Effects of Pimobendan (But Not Amrinone) Are Preserved at Rest and During Exercise in Conscious Dogs with Pacing-Induced Heart Failure

Nobuyuki Ohte, Che-Ping Cheng, Makoto Suzuki and William C. Little
Journal of Pharmacology and Experimental Therapeutics July 1997, 282 (1) 23-31;
Nobuyuki Ohte
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Che-Ping Cheng
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Makoto Suzuki
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William C. Little
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Abstract

We compared the effects of pimobendan (0.25 mg/kg i.v.), a Ca++ sensitizer, with some phosphodiesterase-III inhibition effects, and amrinone (1 mg/kg plus 10 μg/kg/min i.v.), a PDE-III inhibitor, on left ventricular (LV) systolic and diastolic performance, both at rest and during exercise, in seven conscious dogs before and after pacing-induced congestive heart failure (CHF). Before CHF, under resting conditions, both pimobendan and amrinone caused a similar significant decrease in left ventricle size and end-systolic pressure, arterial elastance, and the time constant of LV relaxation. Similar results were obtained during exercise. Both agents also produced a similar increase in E ES, the slope of the LV end-systolic pressure-volume relation (3.4 ± 1.5 vs.4.2 ± 1.1 mm Hg/ml; amrinone vs. pimobendan). After CHF, the vasodilatory effects of amrinone and pimobendan were preserved both at rest and during exercise; however, the inotropic actions were different. After CHF, pimobendan increased E ES(3.9 ± 0.5 vs. 5.7 ± 0.4 mm Hg/ml, P < .05), decreased the time constant of LV relaxation, increased the maximum rate of LV filling (37 ± 19 ml/sec) (P < .05) and produced a downward shift of the early diastolic portion of LV pressure-volume loop. Pimobendan also augmented LV contractile performance during CHF exercise. In contrast, after CHF, amrinone no longer produced a positive inotropic effect. Amrinone improved LV relaxation and filling, both at rest and during exercise after CHF, but significantly less than pimobendan. We conclude that after CHF, the cardiac response to a PDE-III inhibitor is attenuated, but the response to Ca++ sensitizer is preserved. Thus, after CHF, pimobendan is more effective than amrinone in enhancing LV contractile state, LV relaxation and LV filling both at rest and during exercise.

Footnotes

  • Send reprint requests to: William C. Little, M.D., Cardiology Section, Bowman Gray School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157-1045.

  • ↵1 A preliminary report was presented at the Scientific Sessions of the American Heart Association, November, 1996. Study supported in part by grants from NIH (HL45258 and HL42364) and the American Heart Association.

  • Abbreviations:
    CHF
    congestive heart failure
    PDE-III
    phosphodiesterase-III
    LV
    left ventricle
    LA
    left atrium
    P-V
    pressure-volume
    PES
    end-systolic pressure
    PED
    end-diastolic pressure
    TSR
    total systemic resistance
    T
    time constant of LV relaxation
    VLV
    left ventricular volume
    VES
    left ventricular end-systolic volume
    VED
    end diastolic volume
    SW
    left ventricular stroke work
    EA
    arterial elastance
    PVA
    LV pressure-volume area
    SV
    stroke volume
    EES
    slope of the LVP ES-V ES relation
    dV/dtmax
    maximum rate of LV filling
    MSW
    slope of the SW-V EDrelation
    dE/dtmax
    slope of thedP/dt max-V ED relation
    • Received December 20, 1996.
    • Accepted March 21, 1997.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics
Vol. 282, Issue 1
1 Jul 1997
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OtherCARDIOVASCULAR PHARMACOLOGY

The Cardiac Effects of Pimobendan (But Not Amrinone) Are Preserved at Rest and During Exercise in Conscious Dogs with Pacing-Induced Heart Failure

Nobuyuki Ohte, Che-Ping Cheng, Makoto Suzuki and William C. Little
Journal of Pharmacology and Experimental Therapeutics July 1, 1997, 282 (1) 23-31;

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OtherCARDIOVASCULAR PHARMACOLOGY

The Cardiac Effects of Pimobendan (But Not Amrinone) Are Preserved at Rest and During Exercise in Conscious Dogs with Pacing-Induced Heart Failure

Nobuyuki Ohte, Che-Ping Cheng, Makoto Suzuki and William C. Little
Journal of Pharmacology and Experimental Therapeutics July 1, 1997, 282 (1) 23-31;
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