Effects of acute distension of the left ventricle on heart rate were studied in conscious, instrumented dogs. In intact dogs, increasing left ventricular (LV) systolic pressure by a maximum of 77.6 ± 3.6 mmHg from a control of 123.1 ± 3.6 and LV end-diastolic pressure by a maximum of 24.1 ± 2.0 mmHg from a control of 8.5 ± 1.3 did not result in any consistent change in heart rate. Reduction of arterial pressure with sodium nitroprusside caused an increase in heart rate to 143.9 ± 13.8 beats/min. With baroreceptors unloaded, increasing LV pressure by a similar degree as in the control group now resulted in consistent and significant bradycardia. Removal of arterial baroreceptors in a final group of dogs abolished the baroreflex. Increasing LV pressure by aortic stenosis now resulted in a stimulus-dependent decrease in heart rate that was significantly greater than that in the nitroprusside group. Both administration of atropine and bilateral cervical vagotomy abolished bradycardia. The second part of this study was concerned with effects of increases in LV inotropic state on heart rate change evoked by aortic stenosis. Each group was infused with intracoronary epinephrine. Infusion of epinephrine (12.5-50.0 ng·kg-1·min-1) significantly increased LV dP/dt without any significant change in heart rate or mean arterial blood pressure. Aortic stenosis during epinephrine infusion did not result in any significant difference in heart rate responses in any group studied. It is concluded that LV distension can cause a reduction in heart rate that is opposed by the presence of arterial baroreceptors and that increases in LV myocardial contractility do not have any effect on the magnitude of this response.
|Original language||English (US)|
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|Issue number||2 (19/2)|
|State||Published - 1986|
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Physiology (medical)