Cardiac performance: Significance of the Frank-Starling mechanism at low inotropy

Abstract

Stroke volume falls during elevation of systemic blood pressure after blockade of β-adrenergic receptors with propranolol in dogs. To examine the importance of the Frank-Starling mechanism in the stroke volume regulation, systolic left ventricular pressure (LVP) was raised about 25 and 50 mmHg by intravenous infusion of angiotensin in closed-chest and open-chest dogs after infusion of propranolol. This experiment was performed at three levels of blood volume. Blood volume was raised by saline/dextran infusion until end-diastolic LVP exceeded 15-20 mmHg and the Frank-Starling mechanism was beyond its compensatory range. A rise in systolic LVP by 50 mmHg reduced stroke volume by 30-40% at the highest blood volume and by about 20% before blood volume expansion. Recordings of myocardial chord length by ultrasonic technique in open-chest dogs showed that about 40% of the rise in stroke volume during saline/dextran infusion at control blood pressure was due to end-diastolic dilation alone (geometric factor) and 60% to increased myocardial shortening (Frank-Starling mechanism proper). We conclude that under conditions of low inotropy the reduction in stroke volume during elevation of blood pressure is halved and the stroke volume increasing effect of blood volume expansion is more than doubled by the compensatory effects of the Frank-Starling mechanism.

Key Words:

• angiotensin
• blood volume
• calcium
• left ventricular volume and pressure
• propranolol