SUMMARYPerfusion in situ of the placenta of intact or previously parathyroidectomized fetal lambs has been used to assess the ability of three mid-molecule fragments of the human parathyroid hormone-related protein (PTHrP)

SUMMARYThis research was designed to compare coronary, carotid and aortic arch baroreceptors in terms of the ranges of pressures required to elicit reflex vascular responses and the possible differences between the responses to pulsatile and non-pulsatile stimuli. Dogs were anaesthetized with a-chloralose, artificially ventilated and the chests opened wide. A perfusion circuit allowed independent control of pressures distending the three baroreceptor regions. A cardiopulmonary bypass and ventricular fibrillation prevented cardiac pulsations from influencing coronary baroreceptor pressure. The caudal region of the animal was perfused at constant flow and vascular resistance responses were assessed from changes in perfusion pressure. Only tests in which the overall response exceeded 3 kPa (22.5 mmHg) were analysed. Reflex responses were obtained to significantly lower coronary pressures than were required to induce responses from other regions. The inflexion points of the stimulus-response curves for pulsatile coronary, carotid and aortic pressures were 10.5 + 0 6, 15 5 + 1 8 and 16 4 + 1 7 kPa (79 + 5, 116 + 14 and 123 + 13 mmHg, respectively; values are means + S.E.M.). When the responses to pulsatile stimuli were compared with those to non-pulsatile stimuli, it was noted that for the carotid receptors, lower pressures were required to induce responses (inflexion pressure less) and the slope of the stimulus-response curve was less. Pulsatile aortic pressures induced a parallel (downward) displacement of the curve but no change in inflexion point or slope. The coronary baroreceptor stimulus-response relationship was unaffected by pulsatility. These results show differences between the characteristics of the three baroreceptors with coronary receptors being unaffected by pressure pulsatility but likely to be of importance in hypotensive situations.

SUMMARYIn chloralose-anaesthetized dogs, pressures applied to coronary, carotid and aortic baroreceptors were changed independently and the resulting reflex vascular responses were determined. Increases in pressure to each group of baroreceptors resulted in reflex vasodilatation; the maximal responses to distension of carotid and coronary baroreceptors were significantly larger than those to aortic receptors, but not different from each other. Increases in pressure in all three regions induced maximal responses at similar times from the onset of the pressure stimulus. However, the time for recovery of vascular resistance following a decrease in baroreceptor pressure differed. Vasoconstriction following a period of coronary hypertension occurred slowly, requiring 70 s for 90 % of the response to develop. This was significantly longer than the corresponding times for carotid and aortic receptors (about 28 s). The rate of vasoconstriction in response to coronary baroreceptor unloading was influenced by the period for which the pressure stimulus was applied and vasoconstriction was even slower when the pressure stimulus had been maintained for 8 min. The mechanism responsible for delaying the vasoconstriction following a period of coronary hypertension is not known, but this effect may have important implications for the control of arterial blood pressure.

In chloralose‐anaesthetized, artificially ventilated dogs, the splenic pedicle was tied and the carotid sinuses were vascularly isolated and perfused at controlled pressures. In Series 1 experiments, the hepatosplanchnic circulation was perfused through the abdominal aorta with a tie on the aorta separating it from the caudal circulation, which was perfused through the femoral arteries. The two circulations were drained from cannulae in the inferior vena cava and the femoral veins, with a tie on the inferior vena cava separating the two. In Series 2, the splanchnic circulation drained from the portal vein. In both series, inflows and outflows were measured and integrated to derive volume changes. Capacitance responses were assessed during constant flow, and capacitance plus passive responses were obtained during constant pressure perfusion. In Series 1, an increase in carotid sinus pressure (from 8 to 26 kPa) during constant flow and constant pressure perfusion increased hepatosplanchnic volume by 2.5 and 5.7 ml (kg body weight)−1, respectively. The volume of the subdiaphragmatic circulation did not increase during constant flow, but during constant pressure it increased by 2.0 ml (kg body weight)−1. In Series 2, increasing carotid pressure during constant flow and constant pressure increased the volume of the splanchnic circulation by 0.5 and 4.2 ml (kg body weight)−1, respectively. These results confirm that carotid baroreceptor stimulation causes larger volume changes during constant pressure perfusion than during constant flow perfusion. Also, the active capacitance change in the splanchnic circulation is small in relation to the passive response. We propose that in dogs (following splenic ligation), the major active capacitance control is from the liver. However, large passive changes in splanchnic volume occur due to changes in flow.

This was undertaken to determine whether distension of the subdiaphragmatic veins results in reflex vasoconstriction and interacts with the carotid baroreflex. In alpha-chloralose-anesthetized open-chest dogs, a perfusion circuit controlled carotid and thoracic aortic pressures, splanchnic and limb blood flows, and cardiopulmonary blood flows. At carotid sinus pressures below approximately 90 mmHg, increases in splanchnic pressure of 7 mmHg or more resulted in increases in vascular resistance in both the splanchnic and limb circulations; there was no response at higher carotid pressures. At high venous pressures, the average maximum gains of the carotid baroreflex for splanchnic and limb resistance responses were increased by 106 and 67%, respectively. The responses were not abolished by cutting the vagal or phrenic nerves but were prevented by cutting the splanchnic nerves and, for the limb, the sciatic and femoral nerves. These results suggest that splanchnic congestion, by causing vasoconstriction and augmentation of the carotid baroreflex, may be important in the maintenance of blood pressure during gravitational stress.