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Abstract
During adrenergic inotropic stimulation of the heart, an increase in aortic blood pressure (AP) results in a further rise in mechanical activity of the heart, as evidenced by increased rate of rise of left ventricular pressure (dP/dt) and cardiac output (CO). The present study, carried out in anesthetized dogs, showed qualitatively similar results during non-adrenergic inotropic stimulation of the heart with calcium-gluconate or glucagon. The rise in myocardial oxygen consumption (MV˙O2) by raised AP, however, differed during adrenergic and non-adrenergic stimulation. In the presence of calcium-gluconate or glucagon, the rise in MV˙O2could be solely related to changes in myocardial contractility and tension, as both plasma-free fatty acids (FFA) and myocardial uptake of FFA remained low. In contrast, with adrenergic stimulation by isoproterenol, there was the additional influence of high myocardial uptake of FFA on MV˙O2. The present study indicates lower oxygen cost for similar hemodynamic performance with non-adrenergic stimulation of the heart – a finding which may be advantageous in the treatment of ischemic heart disease.