1976 Volume 39 Issue 12 Pages 1357-1363
In order to study the therapeutic implication of controlling heart rate in the treatment of aortic regurgitation, the present experimental study was carried out on in situ dog heart with an aorto-ventricular shunt. Methods : A bilateral transsternal thoracotomy was per-formed in 10 dogs anesthetized with sodium pentobarbital. As illustrated in Fig. 1A, the left ventricle was connected with the aorta through a circuit which involved a flow probe and a check-ball-valve. The latter permitted flow to occur only from the aorta to the left ventricle. A flow probe was also placed around the aortic root. After crushing the sinus node, the heart was paced electrically. As the heart rate was increased in steps, total cardiac output, regurgitant flow rate, effective cardiac output, aortic pressure, left ventricular end-diastolic pressure and PO2, PCO2, and pH of coronary sinus blood were measured. Results: The hemodynamic effects of the change of heart rate were studied on the hearts with the shunt opened (regurgitation group) and those with the shunt closed (control group). The opening of the shunt resulted in the regurgitation with a regurgitant ratio of approximately 33% at the heart rate of 100 beats per min (Fig. 3B). In the regurgitation group, total cardiac output remained unchanged until the heart rate was increased to 180 beats per min and then tended to decrease (Fig. 2) while the regurgitant flow and regurgitant ratio continued to decrease (Fig. 3A, 3B). The effective cardiac output was maximal in the heart rate range between 120 and 160 beats per min (Fig. 4). The shortening of the duration of diastole per min and the elevation of aortic diastolic pressure due to heart rate increase were more profound in the regurgitation group than in the control group (Fig. 5, 6). No decrease of coronary sinus blood PO2 was observed in both groups unless the heart rate was raised beyond 180 beats per min (Fig. 7).
