Left ventricular function during acute elevation of aortic blood pressure in dogs.
Cardiac responses to mechanical constriction of the aorta proximal and distal to the arch arteries and to intravenous infusion of angiotensin were examined in open-chest atropinized dogs during continuous recording of left ventricular and aortic dimensions by means of ultrasonic elements. Proximal constriction reduced stroke volume by 18% both before and during isoproterenol infusion without changing left ventricular end-diastolic pressure, dimensions, or contractility, (dP/dt)IP; angiotensin induced less pronounced increments in stroke volume and end-diastolic volume. By combining proximal constriction with saline-dextran infusion, stroke volume and end-diastolic volume increased as during distal constriction. These results indicate that differences in preload account for the differences in stroke volume responses to proximal and distal aortic constriction. We propose that increased preload is caused by redistribution of blood from capacitance vessels rather than retention secondary to cardiac decompensation.
D000804:Angiotensin II; D000818:Animals; D001011:Aorta / Q000503:physiopathology*; D001794:Blood Pressure; D001810:Blood Volume; D002302:Cardiac Output; D003250:Constriction; D003251:Constriction, Pathologic; D004285:Dogs; D005260:Female; D006321:Heart / Q000503:physiopathology*; D006339:Heart Rate; D006352:Heart Ventricles / Q000503:physiopathology; D006439:Hemodynamics; D006973:Hypertension / Q000139:chemically induced / Q000209:etiology / Q000503:physiopathology*; D007545:Isoproterenol; D008297:Male; D009200:Myocardial Contraction
D000804:Angiotensin II; D007545:Isoproterenol