Anatomical and functional characteristics of carotid sinus stimulation in humans.
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Transmission characteristics of pneumatic pressure to the carotid sinus were evaluated in 19 subjects at rest and during exercise. Either a percutaneous fluid-filled (n = 12) or balloon-tipped catheter (n = 7) was placed at the carotid bifurcation to record internal transmission of external neck pressure/neck suction (NP/NS). Sustained, 5-s pulses, and rapid ramping pulse protocols (+40 to -80 Torr) were recorded. Transmission of pressure stimuli was less with the fluid-filled catheter compared with that of the balloon-tipped catheter (65% vs. 82% negative pressure, 83% vs. 89% positive pressure; P < 0.05). Anatomical location of the carotid sinus averaged 3.2 cm (left) and 3.6 cm (right) from the gonion of the mandible with a range of 0-7.5 cm. Transmission was not altered by exercise or Valsalva maneuver, but did vary depending on the position of the carotid sinus locus beneath the sealed chamber. These data indicate that transmission of external NP/NS was higher than previously recorded in humans, and anatomical variation of carotid sinus location and equipment design can affect transmission results. (+info)
Reflex vascular responses to independent changes in left ventricular end-diastolic and peak systolic pressures and inotropic state in anaesthetised dogs.
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1. Ventricular mechanoreceptors are known to exist and can when stimulated induce reflex vasodilatation, but the nature of the effective stimuli and the physiological role of the reflex remain to be established. 2. Dogs were anaesthetised with chloralose and a cardiopulmonary bypass established. Ventricular pressures were separated from those in the aortic root and coronary arteries by a balloon inflated in the ventricular outflow tract. Ventricular filling was controlled by adjusting the rate of inflow of blood through an apical cannula and peak pressure by regulating the outflow pressure from the same cannula. Carotid and aortic pressures were also controlled and vascular resistance was assessed from changes in perfusion pressure (constant flow conditions) to the descending abdominal aorta. 3. Increased coronary or carotid sinus pressure induced a significant vasodilatation. Changes in ventricular peak systolic pressure, without associated changes in end-diastolic pressure, had no significant effect on vascular resistance. In contrast, changes in end-diastolic pressure did induce vasodilatation that, although small, was proportional to the magnitude of the end-diastolic pressure change. 4. Changes in ventricular inotropic state induced by dobutamine infusion or by stimulation of efferent cardiac sympathetic nerves did not induce significant responses. Furthermore, the combined effects of reduced ventricular filling and increased inotropic state were also ineffective in inducing responses. 5. We conclude that, to induce reflex responses, the only effective stimulus to ventricular mechanoreceptors was an increase in filling. Compared with other mechanoreflexes, however, responses to ventricular distension were small and seem unlikely to be of importance except perhaps during abnormal ventricular distension. (+info)
Potencies of doxapram and hypoxia in stimulating carotid-body chemoreceptors and ventilation in anesthetized cats.
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The effects of doxapram on carotid chemoreceptor activity and on ventilation (phrenic-nerve activity) were tested before and after denervation of the peripheral chemoreceptors in cats. Doxapram was found to be a potent stimulus to the carotid chemoreceptors; the stimulation produced by 1.0 mg/kg doxapram, iv, equalled that produced by a Pao2 of 38 torr. Doxapram also increased phrenic-nerve activity in doses as low as 0.2 mg/kg, iv. After denervation of the peripheral chemoreceptors, doxapram in doses as large as 6 mg/kg failed to stimulate ventilation. It is concluded that (in anesthetized cats) doxapram in doses of less than 6 mg/kg increases ventilation by direct stimulation of the carotid, and, probably, the aortic, chemoreceptors, not by a direct effect on the medullary respiratory center. (+info)
Diverging respiratory effects of serotonin and nicotine in vagotomised cats prior to and after section of carotid sinus nerves.
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Respiratory effects of intravenous serotonin and nicotine were investigated prior to and after bilateral neurotomy of the carotid sinus nerves (CSNs) in eight pentobarbitone/chloralose-anaesthetised, bilaterally vagotomised and superior laryngeal nerves-sectioned cats. Injection of 188 nmol kg(-1) serotonin (hydrogen oxalate salt, 50 microg x kg(-1)) prior to and after CSNs section induced an expiratory apnoea of, respectively, 7.9 +/- 1.25 s and 8.3 +/- 1.6 s duration (mean +/- S.E.M.) in, respectively, five and three of those cats. In all cats, the serotonin challenge produced a period of accelerated breathing (P < 0.05) both prior to and after section of CSNs. Injection of a 433 nmol nicotine bolus (hydrogen tartrate salt, 200 microg) increased tidal volume by 25 +/- 8% in cats with intact CSNs (P < 0.01), but decreased it by 13 + 10% (P < 0.05) after CSNs section. Nicotine, but not serotonin, transiently increased mean arterial blood pressure in our cats, which rise was delayed by CSNs cut. Results of this study indicate that the respiratory response to serotonin occurs beyond carotid body chemoreceptors in vagotomised cats, and suggest that the volume response to intravenous nicotine depends qualitatively on carotid body chemoreceptor input in this experimental model. (+info)
Cardiovascular effects of static carotid baroreceptor stimulation during water immersion in humans.
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We hypothesized that the more-pronounced hypotensive and bradycardic effects of an antiorthostatic posture change from seated to supine than water immersion are caused by hydrostatic carotid baroreceptor stimulation. Ten seated healthy males underwent five interventions of 15-min each of 1) posture change to supine, 2) seated water immersion to the Xiphoid process (WI), 3) seated neck suction (NS), 4) WI with simultaneous neck suction (-22 mmHg) adjusted to simulate the carotid hydrostatic pressure increase during supine (WI + NS), and 5) seated control. Left atrial diameter increased similarly during supine, WI + NS, and WI and was unchanged during control and NS. Mean arterial pressure (MAP) decreased the most during supine (7 +/- 1 mmHg, P < 0.05) and less during WI + NS (4 +/- 1 mmHg) and NS (3 +/- 1 mmHg). The decrease in heart rate (HR) by 13 +/- 1 beats/min (P < 0.05) and the increase in arterial pulse pressure (PP) by 17 +/- 4 mmHg (P < 0.05) during supine was more pronounced (P < 0.05) than during WI + NS (10 +/- 2 beats/min and 7 +/- 2 mmHg, respectively) and WI (8 +/- 2 beats/min and 6 +/- 1 mmHg, respectively, P < 0.05). Plasma vasopressin decreased only during supine and WI, and plasma norepinephrine, in addition, decreased during WI + NS (P < 0.05). In conclusion, WI + NS is not sufficient to decrease MAP and HR to a similar extent as a 15-min seated to supine posture change. We suggest that not only static carotid baroreceptor stimulation but also the increase in PP combined with low-pressure receptor stimulation is a possible mechanism for the more-pronounced decrease in MAP and HR during the posture change. (+info)
Sinoatrial block. Autonomic influences and clinical assessment.
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Seventeen patient with sinoatrial block and 16 healthy volunteers were investigated with recently developed autonomic tests of atrial pacemaker function. Only one patients was found to be entirely normal in comparison with normal subjects, while another patients had supernormal responses. Fifteen patients had reduced responses relative to the controls implying impaired atrial pacemaker function or sinoatrial disease. It is suggested that while in some cases sinoatrial block may be of physiological origin, it is more often due to sinoatrial disease. The latter group are liable to Adams-Stokes syncope and may have additional atricventricular conduction abnormalities. The possible mechanisms and treatment of sinoatrial block are discussed relative to the autonomic and pacemaker function abnormalities described. (+info)
Baroreceptor and chemoreceptor influences on heart rate during the respiratory cycle in the dog.
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1. Brief stimuli were delivered to the carotid chemoreceptors or baroreceptors in dogs anaesthetized with pentobarbitone or chloralose. Chemoreceptor stimulation was achieved by rapid retrograde injections of 0-2-0-5 ml. warmed, CO2-equilibrated saline through a cannula in the external carotid artery. Baroreceptor stimulation was achieved by forceful retrograde injection of 2-5 ml. air-equilibrated saline, or of freshly drawn arterial blood, into the external carotid artery after first clamping the common carotid artery. 2. Brief baroreceptor stimuli had no noticeable effect on breathing. Brief chemoreceptor stimuli had no effect on breathing in some dogs, but in many produced a reflex increase in the depth of inspiration when delivered during inspiration. In these same dogs, brief chemoreceptor stimuli delivered in expiration either prolonged the expiratory pause or evoked an active expiratory effort. 3. Prompt decreases in heart rate were elicited by brief sudden chemoreceptor or baroreceptor stimuli when these were delivered during the expiratory phase of respiration. The stimuli did not modify the control heart rate pattern when delivered during inspiration. If the carotid sinus nerve or the vagus nerves were cut the responses were abolished. 4. Brief chemoreceptor or baroreceptor stimuli remained effective in evoking prompt decreases in heart rate during periods of apnoea in the end-inspiratory position (Hering-Breuer inflation reflex). In periods of apnoea after prolonged artificial hyperventilation the stimuli were sometimes ineffective at first, but were always effective late in the period of apnoea, again producing prompt cardiac slowing. 5. After denervation of the lungs, brief baroreceptor and chemoreceptor stimuli continued to evoke prompt falls in heart rate when given during expiration. When delivered during inspiration the same stimuli were either ineffective, or less effective. (+info)
Responses to stimulation of coronary and carotid baroreceptors and the coronary chemoreflex at different ventricular distending pressures in anaesthetised dogs.
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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. (+info)