Effect of milrinone and atrial pacing on stunned myocardium

Abstract

Stunned myocardium responds pathologically to atrial pacing with a negative staircase in contrast to the positive staircase of intact myocardium. Inotropic stimulation by the phosphodiesterase inhibitor milrinone recruited the functional reserve of stunned myocardium. Milrinone did not restore a positive staircase in stunned myocardium, but power was maintained during atrial pacing. The pathological staircase of stunned myocardium may arise from an impaired availability of cyclic AMP, but the data do not exclude defects in calcium handling, a dysfunction of the sarcoplasmic reticulum, or an impaired Ca-sensitivity of the myofilaments.

Milrinone Administered Before Ischemia or Just After Reperfusion, Attenuates Myocardial Stunning in Anesthetized Swine

“…Schad et al [27] demonstrated that milrinone (bolus dose of 105 mg/kg followed by 5 mg/kg/min) administered from 90 min after reperfusion can improve the contractile function of a stunned myocardium in an open chest swine model. Vandeplassche et al [28] also demonstrated that milrinone was administered cumulatively from 30 min after reperfusion in an open-chest dog model, and a total dose of 160 mg/kg was needed to improve the contractile function of a stunned myocardium significantly compared with the solvent-treated group.…”

A depressão miocárdica pós-isquemia/reperfusão não altera a resposta cardíaca à elevação da freqüência de contrações

“…This interpretation is gaining importance mainly because of convincing demonstrations that the calcium offer to the myoplasm is not altered a few minutes after myocardial reperfusion is started. This hypothesis is yet supported by the fact that the functional capacity of the depressed myocardium may be stimulated by inotropic maneuvers that act on calcium cellular kinetics, such as sympathomimetic amines [8][9][10][11]27 , milrinone 12 , calcium administration 5,13 , postextrasystolic stimulation 9,13 , and postpause stimulation 14 . The reduction in the -dP/dt values after ischemia/reperfusion contradicts the idea that the calcium kinetics is not affected by the ischemia/reperfusion binomial.…”

“…Therefore, postischemia/reperfusion stunned myocardium has been proven not to reduce the intracellular content of the ion 3,4,7 and to preserve the physiological and pharmacological maneuvers that stimulate inotropism by increasing the intracellular content of calcium ([Ca] i ): beta-adrenergic agonists [8][9][10][11] , milrinone 8,12 , calcium administration 5,13 , postpause potentiation 14 , and postextrasystolic potentiation 9,13 . However, the positive inotropic effect depending on heart rate elevation studied in myocardial segments of dogs undergoing regional ischemia has been reported to transform into negative inotropic action after myocardial ischemia/reperfusion 12 . If this inversion of the myocardial response to heart rate elevation is confirmed, the concept of the integrity of calcium kinetics after periods of ischemia/reperfusion should be revised, because, typically, the inotropic action linked to heart rate fluctuations is a physiological maneuver that depends exclusively on calcium kinetics.…”

Stunning and myocardial contractile autoregulation studied on the isolated isovolumic blood‐perfused dog heart

“…1997) and another one focusing cardiac response to ventricular dilation (VD) (Lew 1993) in the stunned myocardium. Schad et al. (1997) concluded that, in the in situ dog heart, stunning inverts the positive inotropic action of normal Bowditch effect.…”

“…To our knowledge, there is only one report on the evaluation of the Bowditch effect (Schad et al. 1997) and another one focusing cardiac response to ventricular dilation (VD) (Lew 1993) in the stunned myocardium.…”