Cardiac dynamics during hemorrhage. Relative unimportance of adrenergic inotropic responses.

We examined, in conscious dogs, the effects of acute hemorrhage on measurements of mean arterial and left ventricular (LV) pressures, LV diameters, LV dP/dt, LV dP/dt/P40, LV dP/dt/ circ, i.e., LV dP/dt divided by LV circumference, and LV dD/dt, i.e., velocity of myocardial fiber shortening. Hemorrhage (30 ml/kg) over 1 hour reduced mean arterial pressure (31 ± 4.3%), LV end-diastolic (21 ± 3.2%) and end-systolic (13 ± 1.6%) diameters, and LV end-diastolic pressure (69 ± 4.6%). Heart rate increased by a maximum of 37 ± 7.5% at 20 ml/kg of blood loss. Indices of myocardial contractility rose slightly (~10%) during the initial normotensive hemorrhage, but then fell. Hemorrhage (30 ml/kg) reduced LV velocity by 31 ± 2.6%, LV dP/dt by 37 ± 2.9%, LV dP/dt/ P40 by 34 ± 3.5%, and LV dP/dt/circ by 17 ± 7.2%. More rapid hemorrhage, 30 ml/kg at a rate of 1 ml/sec, induced similar effects. After /8-adrenergic receptor blockade, the indices of myocardial contractility failed to rise initially and then fell with hemorrhage. The changes in indices of myocardial contractility were only slightly different (~10%) from those in dogs without blockade. Responses of mean arterial pressure and LV end-diastolic diameter to hemorrhage were essentially identical in the presence and absence of either selective /Sior combined /Siand /62-adrenergic receptor blockades. After hemorrhage, 30 ml/kg, when LV end-diastolic diameter was returned to pre-hemorrhage values by aortic constriction in dogs without /S-adrenergic receptor blockade, LV dP/dt returned to, but not significantly above, control levels. Thus, activation of the sympathetic nervous system results in only small increases in cardiac contractility during acute hemorrhage, which are relatively unimportant in cardiovascular control. (Circ Res 50: 705-713, 1982)