Key result
Dobutamine during reperfusion fails to reduce myocardial infarct size versus saline in a rabbit model.
Why the study?
Does dobutamine infusion during reperfusion reduce myocardial infarct size in a rabbit ischemia-reperfusion model?
Does dobutamine infusion during reperfusion reduce myocardial infarct size in a rabbit ischemia-reperfusion model?
In a rabbit ischemia-reperfusion model, an inotropic dose of dobutamine administered during reperfusion did not significantly alter myocardial infarct size, suggesting it does not exacerbate ischemic injury.
Dobutamine during reperfusion shows neutral effect on infarct size in rabbits; leaves open its impact on clinical reperfusion injury.
We examined whether dobutamine infusion during reperfusion modifies myocardial infarct size in a rabbit ischemia-reperfusion model. Prior to the infarct size study, the hemodynamic response to dobutamine 5, 10, and 15 micrograms/kg/min i.v. was evaluated in the rabbit model. Ten micrograms/kg/min of dobutamine increased the left ventricular dp/dt max by 34.0 +/- 4.9% (n = 7) and the myocardial blood flow from 0.86 +/- 0.16 to 2.19 +/- 0.57 ml/min/g without change in the collateral blood flow (n = 4). The heart rate, systolic and diastolic blood pressures were elevated by only 4.7 +/- 1.0%, 9.4 +/- 3.0%, and 8.0 +/- 3.7%, respectively (n = 7). In the infarct size study, a coronary branch was occluded for 30 min and then reperfused. Seventy-two hours after reperfusion, the myocardium supplied by the occluded artery (area at risk, AAR) and the infarcted area were determined by fluorescent particles and histology (hematoxylin-eosin and modified Mallory's staining), respectively. In the dobutamine treated group (DB group), 10 micrograms/kg/min of dobutamine were infused for 30 min starting immediately after reperfusion, and a comparable volume of saline was infused in the control group. Hemodynamic parameters and the size of AAR were comparable in the control and DB groups. Myocardial infarct size, expressed as the percentage of AAR, was 45.1 +/- 3.9% in the control (n = 11) and 40.2 +/- 2.4% in the DB group (n = 10), which was not significantly different. These findings indicated that the inotropic dose of dobutamine administered during reperfusion did not cause myocardial necrosis by disturbing the recovery process of the myocardium from ischemic injury.
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Ooiwa et al. (1989) studied Myocardial ischemia-reperfusion injury (n=21). Dobutamine vs. Saline was evaluated on Myocardial infarct size, expressed as the percentage of area at risk (AAR) (p=not significantly different). Dobutamine infusion during reperfusion did not significantly change myocardial infarct size compared to saline control (40.2% vs 45.1% of the area at risk) in a rabbit model.
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