Cardiac Response to Increased Aortic Pressure Changes in Output and Left Ventricular Pressure Pattern at Various Levels of Inotropy

Abstract

The cardiac effects of raising aortic pressure were studied in thoracotomized dogs, in conscious dogs after implantation of aortic flowmeters, and in anesthetized, intact dogs Mean aortic blood pressure was raised 50–100 mm Hg either by mechanical constriction of the ascending or descending aorta or by intravenous (i.v.) infusion of angiotensin. Reflex bradycardia was avoided by administration of atropine, but the directional changes in cardiac output were similar before and after atropinization. Stroke volume remained unchanged or decreased when aortic pressure was raised in control experiments and after blockade of β-adrenergic receptors with propranolol. In contrast, the response to a similar pressure increase during continuous infusion of a stimulator of adrenergic β-receptors (isoproterenol i.v. at 3–4 μg per minute) was an increase in stroke volume averaging 27.5 per cent in thoracotomized and 20 per cent in conscious dogs. This response was characterized by maintained peak flow, slightly increased ejection time, and a steeper increase in left ventricular pressure (increased dP/dt). Raising aortic pressure in conscious dogs reduced the acceleration of blood into the aorta, on an average, from 6.1 g to 4.6 g. During isoproterenol infusion, a similar pressure rise increased acceleration from 9.8 g to 11.8 g. Similar responses were obtained after blockade of adrenergic α-receptors with phenoxybenzamine, after ganglion blockade with pentolinium tartrate, and after denervation of carotid sinuses. No evidence of a regulation by extracardiac mechanisms was therefore found, and it is concluded that the cardiac response to increased aortic pressure is dependent on the level of inotropy.

Key Words:

• Angiotensin
• afterload
• aortic flow
• blood pressure
• cardiac contractility
• cardiac output
• catecholamines
• inotropy
• propranolol
• ventricular pressure