Effects of norepinephrine on coronary circulation and left ventricular dynamics in the conscious dog.

The effects of norepinephrine (0.1 and 1.0 Mg/kg, iv) on coronary blood flow and resistance, left ventricular pressure and diameter, dP/dt, (dP/dt)/P, and the velocity (Vlso) of myocardial fiber shortening were studied in conscious dogs. When the heart rate was held constant, norepinephrine caused an initial reduction in coronary vascular resistance which was associated with increases in mean arterial blood pressure, systolic left ventricular pressure, end-diastolic diameter, dP/dt, (dP/dt)/P, and Viso . After this brief coronary vasodilator response, a sustained increase occurred in mean coronary vascular resistance (+0.55 ± 0.07 mm Hg/ml min"'), and increases persisted in mean arterial blood pressure (+67 ± 7 mm Hg), left ventricular systolic pressure (+74 ± 6 mm Hg), left ventricular end-diastolic pressure (+4 ± 1 mm Hg), left ventricular internal diameter ( + 1.3 ± 0.3 mm), peak dP/dt ( + 1660 mm Hg/sec), (dP/dt)/P ( + 15 ± 2 sec"), and Viso ( + 11 ± 2 mm/sec); coronary sinus Po2 decreased. Beta-receptor blockade prevented the inotropic effects of norepinephrine, attenuated the early coronary vasodilator effects, and increased the late vasoconstrictor effects. Alpha-receptor blockade abolished the late coronary vasoconstrictor effects of norepinephrine; only dilatation occurred. In contrast to the effects of norepinephrine in conscious dogs without autonomic blockade, norepinephrine (1.0 ^g/kg, iv) failed to produce late coronary vasoconstriction in anesthetized, open-chest dogs; only dilatation occurred. Thus, in the normal, conscious dog, norepinephrine exerts an important coronary vasoconstrictor effect which is sufficiently intense to counteract completely the simultaneous tendency toward metabolic vasodilatation.