Effect of increased alpha-adrenergic activity on the blood pressure/cardiac output relationship in dogs.

The relationship between mean aortic blood pressure (MAP) and cardiac output (CO) was examined in anaesthesized, open-chest dogs during variations in pre-load with and without alpha-adrenergic stimulation with phenylephrine. When phenylephrine increased MAP to 200 mmHg, CO fell greatly and could not be increased by volume expansion. Left ventricular ultrasonic measurements and pressure recordings showed that the Frank-Starling mechanism was maximally activated. During vena cava obstruction CO and MAP fell proportionally. At a lower infusion rate of phenylephrine, MAP increased to 160 mmHg without a great reduction of CO. As in control experiments without phenylephrine infusion, CO could be increased by dextran/saline infusion and lowered about 20% below control by vena cava obstruction with no significant change in MAP; by further caval obstruction CO and MAP fell in proportion. Phenylephrine did not alter the relationship between aortic baroreceptor activity and MAP. The same MAP/CO relationships were obtained before and after bilateral vagotomy and nephrectomy. Caval obstruction and pacing tachycardia resulted in similar MAP/CO relationships despite different effects on left ventricular end-diastolic pressure. Thus, phenylephrine infusion may raise MAP to 200 mmHg but no cardiac reserve is left. During reduction of CO by caval obstruction, peripheral vascular resistance remains constant despite varying baroreceptor activity. At the lower infusion rate of phenylephrine, raising MAP to 160 mmHg, peripheral vascular resistance is constant at low CO, but at high CO the vasoconstrictive effect of phenylephrine is counteracted by a vasodilatory mechanism which seems to be flow-dependent.