The present studies were conducted in conscious, instrumented rats to evaluate measurements of aortic peak flow velocity (PFV) as an index of myocardial contractility. Because our previous studies had characterized/verified procedures to determine pressure-derived indices of contractile function in the anesthetized, ventilated, open-chest rat, we first correlated PFV with (a) maximum rate of left ventricular pressure development (max +dP/dt) and (b) a contractility index derived by dividing max +dP/dt by left ventricular pressure at max +dP/dt [(dP/dt)/P] in anesthetized rats (n = 5). The positive inotropic agent, isoproterenol, given by bolus intravenous injection (0.2 microgram), significantly and concurrently increased dP/dt, (dP/dt)/P, and PFV. The negative inotropic agent, propranolol, given by bolus intravenous injection (2 mg/kg), significantly and concurrently attenuated all of the above measurements. When control, isoproterenol, and propranolol responses were used to calculate multivariate correlation coefficients among dP/dt, (dP/dt)/P, and PFV, r values ranged from 0.74 (PFV vs. dP/dt) to 0.84 (dP/dt vs. (dP/dt)/P) to 0.91 (PFV vs. (dP/dt)/P). A separate group of rats (n = 4) was surgically implanted with ascending aortic blood flow sensors, carotid artery and jugular vein catheters. Intravenous isoproterenol (0.2 microgram, bolus) elicited increased cardiac (heart rate and cardiac output) and decreased peripheral vascular resistance (mean arterial blood pressure) beta-adrenergic receptor agonist effects. Propranolol (2 mg/kg, i.v. bolus) produced hemodynamic effects consistent with cardiovascular beta-adrenergic receptor blockade. Isoproterenol and propranolol had directionally appropriate, and significant effects on PFV in the conscious rat. When compared with PFV values under control conditions in the anesthetized rat, conscious rat values are approximately double those observed under anesthesia; however, the relative PFV responses to isoproterenol and propranolol were not affected. Therefore, the present studies provide evidence that aortic PFV can be utilized as an estimate of heart contractile performance, i.e., myocardial contractility, in the conscious, instrumented rat.

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