Cardiac Mechanisms for Regulating Stroke Volume during Elevation of Aortic Blood Pressure in Dogs

Cardiac output and stroke volume increased during elevation of aortic pressure at high adrenergic activity (constant isoproterenol infusion or stimulation of left stellate ganglion), but fell in control experiments and after propranolol administration, both in open-chest and conscious dogs. To examine the mechanisms involved, myocardial distances and ventricular volumes were measured with ultrasonic and thermodilution techniques, respectively. Enddiastolic volume always increased during elevation of aortic blood pressure. Myocardial shortening increased further at high adrenergic activity and fell in control experiments. The increase in myocardial shortening was not a consequence of increased delivery to the myocardium of circulating catecholamines, as reduction of coronary blood flow to control before elevation of aortic pressure did not reduce stroke volume. It is concluded that the stroke volume response to elevation of aortic blood pressure is the resultant of two effects: 1) a stroke-volume-increasing effect of increased end-diastolic myocardial fiber length (Frank-Starling mechanism); 2) a stroke-volume-reducing effect of reduced myocardial shortening. This balance is changed towards a rise in stroke volume at high adrenergic activity.