Abstract
This study was designed to assess effects of acute apelin administration on cardiac and coronary performance in anesthetized, open‐chest swine. Systemic intravenous administration of pyr‐apelin 13 (3nM to 1μM) did not significantly affect coronary blood flow (0.37 + 0.07 to 0.29 + 0.06 mL/min/g; p=0.93) or myocardial oxygen consumption (46.47 + 8.64 to 36.84 + 5.93 μL O2/min/g; p=0.91). However, pyr‐apelin 13 elicited a dose‐dependent peripheral dilator response as mean aortic pressure was decreased by 12 + 4 mmHg at 1μM pyr‐apelin 13 (p=0.001). Left ventricular pressure volume relationships were assessed to establish the potential inotropic effects of pyr‐apelin 13. No changes in cardiac output (2074 + 347 to 2052 + 185 mL/min; p= 0.96), stroke volume (35 + 2 to 33 + 1 mL; p=0.34) or end systolic pressure volume relationship (Ees 10.55 + 3.78 to 18.23 + 3.84; p = 0.20) were noted in response to pyr‐apelin 13 (3nm to 1μM). Mass spectroscopic analyses of plasma samples at each dose confirmed a ~700 fold increase in plasma apelin concentrations (0.39 + 0.14 to 287.55 + 43.58 ng/mL; p<0.001) with treatment. Taken together, these data support that acute systemic administration of pyr‐apelin 13 dose‐dependently decreases arterial pressure via reductions in systemic vascular resistance, independent of alterations in cardiac inotropic function.
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