Chronic Propranolol Treatment Promotes Left Ventricular Dilation Without Altering Systolic Function After Large Myocardial Infarction in Rats

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Abstract
In rats with chronic myocardial infarction (MI), we have examined the effects of prolonged .beta.-adrenergic blockade with propranolol on left ventricular (LV) performance, weight, and volumes. Sham-operated rats and rats with large MI (> 30%) were evaluated. Four groups of rats were studied: control, sham-operated (n = 12); control, MI (n = 12); propranolol (500 mg/L of drinking water-treated, sham-operated (n = 10); and propranolol treated, MI (n = 10). Treated was started 3 weeks after coronary ligation. After 5-6 weeks, LV, systemic arterial, and right atrial pressures in addition to aortic blood flow before and during volume loading were measured. LV pressure-volume relations were measured ex vivo. The rats with chronic MI demonstrated expected decreases in LV systolic performance and increased LV end-diastolic and right atrial pressures. Propranolol had no independent effect on LV systolic pressure, LV end-diastolic pressure, resting cardiac index, stressed cardiac index during volume loading, peak developed aortic pressure during aortic occlusion, or ejection fraction index in either sham-operated or infarcted rats; however, heart rate was decreased weight/body weight was 2.17 .+-. 0.04 mg/g in control sham-operated rats, which was not different from the propranolol-treated sham-operated rats (2.09 .+-. 0.04 mg/g). The LV weight/body weight was increased (p < 0.01) to 2.21 .+-. 0.08 mg/g in the propranolol-treated MI2 groups from 1.94 .+-. 0.06 mg/g in the control MI group. The LV pressure-volume relation was not altered by propranolol in the sham-operated rats but was shifted to the right by MI. In the propranolol-treated MI rats, the LV pressure-volume relationship was shifted further to the right compared to the control MI group. The results demonstrate that after large MI during chronic propranolol treatment, the LC stroke volume index appears to be maintained by increased ventricular filling secondary to relative bradycardia. The increase in left ventricular filling, however, is not accompanied by an increase in end-diastolic pressure because the left ventricular pressure-volume relation was shifted to the right and the passive chamber compliance increased.