Responses to stimulation of coronary and carotid baroreceptors and the coronary chemoreflex at different ventricular distending pressures in anaesthetised dogs

Stimulation of left ventricular mechanoreceptors was believed not only to exert important effects on the circulation, but also to influence the responses to baroreceptor reflexes. However, most previous work is flawed due to inadequate localisation of stimuli to specific reflexogenic areas. In this study, we applied a discrete stimulus to left ventricular mechanoreceptors to examine other reflexes known to effect the circulation. Dogs were anaesthetised, artificially ventilated and a cardiopulmonary bypass established. The pressure distending the left ventricle was controlled through an apical cannula with the aortic valve obstructed by a balloon. Changes in ventricular systolic and end-diastolic pressure had only a small effect on vascular resistance, assessed as perfusion pressure in the systemic circulation (flow constant). Responses to changes in carotid or coronary pressure or to stimulation of chemosensitive afferents by injecting veratridine into the coronary circulation were always much larger. Responses to stimulation of these reflexes were little affected by the level of stimulus to the ventricular receptors. These experiments confirm that responses to stimulation of ventricular mechanoreceptors are very small and show that they remain small at different levels of input to other baroreceptive regions. There was no evidence of interaction between ventricular mechanoreceptor reflexes and carotid or coronary baroreceptors or ventricular chemosensitive reflexes

Absence of reflex vascular responses from the intrapulmonary circulation in anaesthetised dogs

The aim of this investigation was to determine whether reflex cardiovascular responses were obtained to localised distension of the intrapulmonary arterial and venous circulations in a preparation in which the stimuli to other major reflexogenic areas were controlled and the lung was shown to possess reflex activity. Dogs were anaesthetised with [alpha]-chloralose, artificially ventilated, the chests widely opened and a cardiopulmonary bypass established. The intrapulmonary region of the left lung was isolated and perfused through the left pulmonary artery and drained through cannulae in the left pulmonary veins via a Starling resistance. Intrapulmonary arterial and venous pressures were controlled by the rate of inflow of blood and the pressure applied to the Starling resistance. Pressures to the carotid, aortic and coronary baroreceptors and heart chambers were controlled. Responses of vascular resistance were assessed from changes in perfusion pressures to a vascularly isolated hind limb and to the remainder of the subdiaphragmatic circulation (flows constant). The reactivity of the preparation was demonstrated by observing decreases in vascular resistance to large step changes in carotid sinus pressure (systemic vascular resistance decreased by -40 ± 5 %), chemical stimulation of lung receptors by injection into the pulmonary circulation of veratridine or capsaicin (resistance decreased by -32 ± 4 %) and, in the four dogs tested, increasing pulmonary stroke volume to 450 ml (resistance decreased by -24 ± 6 %). However, despite this evidence that the lung was innervated, increases in intrapulmonary arterial pressure from 14 ± 1 to 43 ± 3 mmHg or in intrapulmonary venous pressure from 5 ± 2 to 34 ± 2 mmHg or both did not result in any consistent changes in systemic or limb vascular resistances. In two animals tested, however, there were marked decreases in efferent phrenic nerve activity. These results indicate that increases in pressure confined to the intrapulmonary arterial and venous circulations do not cause consistent reflex vascular responses, even though the preparation was shown to be reflexly active and the lung was shown to be innervated

Blood mobilization from the liver of the anaesthetized dog

The abdominal circulation contains a high proportion of the total blood volume and this can change either passively in response to changes in vascular distending pressure or actively (termed a capacitance response) to changes in sympathetic nervous activity. The liver is the largest abdominal organ and this study was designed to evaluate its potential contribution to overall vascular capacitance and compliance. In chloralose anaesthetized dogs, the liver was vascularly isolated, perfused through the portal vein and hepatic artery at either constant pressures or constant flows and drained from the hepatic veins at constant pressure. Changes in vascular resistance were assessed from changes in inflow pressures or flows and hepatic blood volume was determined by differences between net inflow and outflow. During constant flow perfusion the change in hepatic volume (capacitance change) in response to supramaximal stimulation of sympathetic nerves at 16 Hz was (mean ± S.E.M.) -2·40 ± 0·61 ml (kg body weight)-1. This response was not significantly different during constant pressure perfusion. The changes in portal venous and hepatic arterial pressures during stimulation at constant flow perfusion were +0·67 ± 0·13 and +4·92 ± 0·67 kPa, respectively. The compliance of the liver, assessed as the change in volume to a change in hepatic venous pressure, was +5·44 ± 0·18 ml kg-1 kPa-1. These results indicate that the liver has a major capacitance role, comparable to that of the canine spleen and, in addition, is highly compliant. No evidence was found to suggest that a sphincter on the hepatic outflow exists. Assuming similar responses occur in humans, who do not possess a large contractile spleen, the liver would be the most important controllable blood reservoir in the body

Reflex responses from the main pulmonary artery and bifurcation in anaesthetised dogs

This study was undertaken to determine the reflex cardiovascular and respiratory responses to discrete stimulation of pulmonary arterial baroreceptors using a preparation in which secondary modulation of responses from other reflexes was prevented. Dogs were anaesthetised with [alpha]-chloralose, artificially ventilated, the chests widely opened and a cardiopulmonary bypass established. The main pulmonary arterial trunk, bifurcation and extrapulmonary arteries as far as the first lobar arteries on each side were vascularly isolated and perfused through the left pulmonary artery and drained via the right artery through a Starling resistance which controlled pulmonary arterial pressure. Pressures distending systemic baroreceptors and reflexogenic regions in the heart were controlled. Reflex vascular responses were assessed from changes in perfusion pressures to a vascularly isolated hind limb and to the remainder of the subdiaphragmatic systemic circulation, both of which were perfused at constant flows. Respiratory responses were assessed from recordings of efferent phrenic nerve activity. Increases in pulmonary arterial pressure consistently evoked increases in both perfusion pressures and in phrenic nerve activity. Both vascular and respiratory responses were obtained when pulmonary arterial pressure was increased to above about 30 mmHg. Responses increased at higher levels of pulmonary arterial pressures. In 13 dogs increases in pulmonary arterial pressure to 45 mmHg increased systemic perfusion pressure by 24 ± 7 mmHg (mean ± S.E.M.) from 162 ± 11 mmHg. Setting carotid sinus pressure at different levels did not influence the vascular response to changes in pulmonary arterial pressure. The presence of a negative intrathoracic pressure of -20 mmHg resulted in larger vascular responses being obtained at lower levels of pulmonary arterial pressure. This indicates that the reflex may be more effective in the intact closed-chest animal. These results demonstrate that stimulation of pulmonary arterial baroreceptors evokes a pressor reflex and augments respiratory drive. This reflex is likely to be elicited in circumstances where pulmonary arterial pressure increases and the negative excursions of intrathoracic pressure become greater. They are likely, therefore, to be involved in the cardio-respiratory response to exercise as well as in pathological states such as pulmonary hypertension or restrictive or obstructive lung disease