The influence of left ventricular pressure on the vascular responses to changes in carotid sinus pressure in anaesthetized dogs.

The aim of this study was to determine whether the degree of stimulation of left ventricular receptors influenced the sensitivity of the carotid sinus baroreceptor reflex. In anaesthetized dogs, the stimulus to left ventricular receptors was changed by changing aortic root and hence ventricular systolic pressure, using a preparation in which the applied pressure did not distend the aortic arch and in which left atrial pressure was controlled. A large step increase in either carotid or left ventricular pressure resulted in vasodilatation both in a perfused hindlimb and in the remainder of the systemic circulation and resulted in a reduction in the response to a change in pressure in the other area. The stimulus-response curves, relating limb and systemic perfusion pressures to small step changes in carotid sinus pressure, were displaced downwards at high left ventricular pressures. However, the curves remained parallel indicating the absence of an interactive effect. These results indicate that the vascular responses to changes in carotid and ventricular pressures show simple additive summation.

The effects of changes in left ventricular pressure on respiratory activity in anaesthetized dogs.

This study was undertaken to determine whether moderate increases in left ventricular systolic pressure in anaesthetized dogs result in changes in respiratory activity. Left ventricular systolic pressure was changed using a preparation in which the applied pressure did not distend the aortic arch and in which left atrial and carotid sinus pressures were held constant. The systemic circulation was perfused at constant flow and respiratory activity was assessed from the phrenic electroneurogram. Increases in aortic root and left ventricular systolic pressures resulted in a decrease in arterial perfusion pressure, no significant change in heart rate and a decrease in phrenic nerve activity. These responses differed from those to changes in carotid sinus pressure, which were decreases in perfusion pressure and heart rate but no significant steady-state change in phrenic activity. Responses to changes in ventricular pressure were obtained to each small step between 16 and 28 kPa (120 and 210 mmHg). Following cervical vagotomy, changes in ventricular pressure resulted in neither respiratory nor vascular responses. These results indicate that left ventricular receptors may play a role in the control of respiration.

The absence of cardiovascular and respiratory responses to changes in right ventricular pressure in anaesthetized dogs.

1. This study was undertaken to determine whether physiological changes in pressure localized to the right ventricle result in reflex cardiovascular or respiratory responses. 2. Right ventricular systolic pressure was changed using a preparation in which right atrial and carotid sinus pressures were held constant. The pulmonary and hence the systemic circulation were perfused at constant flow. Vascular resistance and respiratory activity were assessed from the systemic arterial pressure and the phrenic electroneurogram. 3. Changes in right ventricular systolic pressure did not result in any consistent changes in heart rate, systemic arterial blood pressure or phrenic nerve activity. 4. Expected responses occurred to changes in the stimuli to carotid baroreceptors and chemoreceptors, distension of pulmonary arterial baroreceptors, and injections of veratridine into the left ventricle and pulmonary circulation. This suggests that the absence of responses to right ventricular distension was unlikely to have been due to damage to nervous pathways. 5. These results indicate that it is unlikely that there are reflexes arising from the right ventricle which have a major role in cardiovascular or respiratory control.

Reflex responses of vascular resistance in anaesthetized dogs to independent changes in ventricular systolic pressure and cardiac inotropic state.

Responses of systemic arterial perfusion pressure to changes in ventricular systolic pressure were determined before and after administration of dobutamine, then after propranolol, to determine whether the effective stimulus to left ventricular receptors was the change in ventricular systolic pressure or inotropic state. The results showed that increases in ventricular systolic pressure resulted in reflex vasodilatation which was unaffected by inotropic state, indicating that changes in ventricular systolic pressure provided the more potent stimulus.

Reflex vascular responses to changes in left ventricular pressure in anaesthetized dogs.

In dogs anaesthetized with chloralose, changes in left ventricular systolic pressure were induced using a preparation in which the pressure changes did not distend the aortic arch and in which left atrial and carotid sinus pressures were held constant. The systemic circulation was perfused at constant flow and drained from the venae cavae at constant pressure. An increase in left ventricular systolic pressure caused reflex dilatation of systemic resistance and capacitance vessels as indicated by decreases in arterial perfusion pressure and venous outflow. Responses were obtained when ventricular systolic pressure changed between 16 and 28 kPa (120-210 mHg). Responses to changes in ventricular pressure were reduced when the carotid sinuses were perfused at high pressures. These results indicate that changes in pressure in the left ventricle result in reflex changes in vascular resistance and capacitance and that responses are obtained to changes in ventricular pressure over a physiological range.