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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of propofol (P), methohexitone (M) and isoflurane (I) on the baroreceptor reflex were studied in a cat model in which the blood pressure in a bilateral isolated carotid sinus preparation was artificially varied between 50-200 mmHg. The influence from aortic and cardiopulmonary baroreceptors was excluded by vagotomy. With basal chloralose anaesthesia as control, the investigated anaesthetics were used in doses corresponding to MAC 0.5 and 1.0. The maximum change in systemic mean arterial pressure (MAP) and heart rate (HR) following a defined increase in carotid sinus pressure was used as an index of baroreceptor reflex sensitivity. Compared to control, M and I anaesthesia were associated with significant depression of baroreceptor reflex sensitivity at the high dose (corresponding to MAC 1.0), and during I anaesthesia also at the low dose (MAC 0.5). The baroreceptor reflex sensitivity was maintained during propofol anaesthesia. The carotid sinus pressure interval at which the maximum changes in MAP could be elicited, was significantly higher during M than during P. This indicates resetting of the baroreflex.
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PMID:The effects of propofol, methohexitone and isoflurane on the baroreceptor reflex in the cat. 146 15

We have previously demonstrated a decrease in baroreceptor discharge sensitivity in dogs with experimental heart failure. In the present study, we determined the sensitivity of the carotid sinus baroreceptor reflex in dogs with pacing-induced heart failure. The carotid sinus baroreceptor reflex sensitivity was determined by pressurizing one carotid sinus with all other baroreceptor and cardiopulmonary receptor inputs removed. The data were analyzed by plotting carotid sinus pressure-mean arterial pressure curves and carotid sinus pressure-renal sympathetic nerve activity curves in the two groups of dogs. The peak arterial pressure during carotid hypotension was significantly depressed in dogs with heart failure compared with normal dogs (107.1 +/- 5.7 versus 139.8 +/- 7.0 mm Hg, p less than 0.001). Mean arterial pressure range, renal sympathetic nerve activity range, and peak slope were significantly decreased in the heart-failure group. To determine if this depression was completely due to depression of baroreceptor discharge per se, or to alterations in central or end-organ responsiveness, similar experiments were performed by stimulating the carotid sinus nerve and evaluating frequency, voltage, and duration of stimulation on the resultant mean arterial pressure and renal sympathetic nerve activity. As was the case with carotid sinus pressurization, electrical stimulation caused a significantly smaller change in mean arterial pressure in heart-failure dogs compared with the normal dogs. However, there was no significant difference between normal and heart-failure dogs for the renal sympathetic nerve activity-electrical stimulation curves. These data strongly suggest that the depressed carotid sinus baroreceptor reflex in heart failure is not solely the result of depressed baroreceptor responsiveness but may be related to poor end-organ responses and normal central control of renal sympathetic outflow.
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PMID:Carotid sinus baroreceptor reflex in dogs with experimental heart failure. 201 93

Blood pressure and heart rate often increase during cocaine intoxication, but the mechanisms of these cardiovascular responses are poorly understood. The most often suggested theories are central nervous system mechanisms involving the blockade of neuronal transmitter uptake. Cocaine also has potent local anesthetic properties, and in this study we tested the possible role of peripheral actions of cocaine at baroreceptor afferents. Single fiber baroreceptors were recorded using an in vitro preparation of the rat aortic arch. Diameter, pressure, and baroreceptor discharge were recorded. Cocaine perfused through the lumen of the aortic arch at a suprathreshold pressure reduced baroreceptor discharge within 90 s of entering the lumen of the aorta. Slow ramps of pressure elicited complete pressure- and diameter-discharge curves every 5 min. Beginning at about 1 microM, cocaine inhibited baroreceptor function; threshold increased, the maximum discharge decreased, and at 100 microM cocaine, all discharge ceased. The vasodilator nitroprusside or the alpha 1-adrenoreceptor antagonist prazosin did not affect baroreceptor responses to cocaine. In in vivo tests in rabbits, cocaine that perfused through a vascularly isolated carotid sinus reduced the slope of the baroreflex relationship between carotid sinus pressure and systemic mean arterial pressure. Significant depression of baroreceptor function was found at concentrations similar to the plasma cocaine levels measured in clinical studies. The local anesthetic properties of cocaine may be involved in baroreceptor effects. Our studies suggest a possible contributing role of a new site of action of cocaine outside the central nervous system. Compromise of baroreceptor reflexes could facilitate the development of serious cardiovascular complications associated with cocaine abuse.
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PMID:Cocaine inhibits baroreflex control of blood pressure by actions at arterial baroreceptors. 233 Oct 13

Several laboratories have shown that electrical stimulation in the posterior hypothalamus inhibits the baroreceptor reflex. However, the results of these studies are difficult to interpret since it is not known if the attenuation of the baroreflex results from activation of axons of passage or from stimulation of hypothalamic cell bodies. The purpose of this study was to determine the effects of chemical stimulation of posterior hypothalamic neurons upon the baroreflex. Arterial baroreceptors were activated by increasing the pressure in an isolated carotid sinus in anesthetized cats and by an increased arterial pressure following intravenous injection of phenylephrine in both anesthetized cats and rats. The baroreceptor reflex was evaluated before and after a GABA antagonist (picrotoxin) was microinjected into the posterior hypothalamus. The bradycardia, but not the depressor response, elicited by increasing carotid sinus pressure was attenuated after unilateral microinjections of picrotoxin into the posterior hypothalamus. In addition, the heart rate response to a phenylephrine-evoked rise in arterial pressure was reduced after picrotoxin was microinjected in both the cats and the rats. Microinjection of a GABA agonist (muscimol) into the same hypothalamic site returned resting heart rate and arterial pressure to levels seen prior to picrotoxin. These results show that the depression of the bradycardia produced by hypothalamic stimulation results from activation of cell bodies in the posterior hypothalamus. This hypothalamic effect upon the baroreflex bradycardia may involve a GABAergic mechanism.
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PMID:A GABAergic mechanism in the posterior hypothalamus modulates baroreflex bradycardia. 338 68

In this study we determined if there are any alterations in carotid sinus baroreceptor discharge in a model of heart failure in the dog. The left carotid sinus was isolated and perfused at 100 mmHg with a modified Krebs-Henseleit solution. Two groups of dogs were used: a normal group and a group with a chronic aorto-caval fistula (a.v.f.) of up to 20 weeks duration. The a.v.f. group had a significantly elevated heart rate and left ventricular end diastolic pressure as well as an increased arterial pulse pressure compared to normals. However, mean arterial pressure measured in the aortic arch was not significantly different. Carotid sinus pressure-discharge curves were constructed during increases in carotid sinus pressure by steps and by ramps of pressure change up to 200 mmHg/s. Carotid sinus diameter was also measured using sonomicrometer crystals. In six dogs from each group the sodium, potassium and water content of the right carotid sinus was measured. Several parameters of second order polynomial curves that were fitted to the data were compared between the two groups for step and ramp increases in pressure. These included maximum baroreceptor gain, threshold pressure and plateau pressure. Baroreceptor gain was significantly lower in the a.v.f. group for the step and lowest ramp rate pressure changes. Threshold pressure was significantly higher for the a.v.f. group for steps and the three slowest ramp rates. Plateau pressures were significantly higher for the steps and lowest ramp rate. The carotid sinus strain that was produced at any given carotid sinus pressure was not significantly different between the two groups. In addition, there was no difference in the sodium, potassium or water content of the carotid sinus between the two groups. It was concluded that there is a depression of the static discharge characteristics in this model of heart failure which is not due to an alteration in electrolyte or water content or to the compliance of the carotid sinus.
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PMID:Static and dynamic responses of carotid sinus baroreceptors in dogs with chronic volume overload. 409 85

Drugs interfering with sympathetic tone may result in depression of the function of the sinus node, especially in patients with disease of the sinus node. In 11 patients presenting with palpitations, vertigo, or syncope, the heart rate, the recovery time of the sinus node, the carotid sinus pressure slowing, and the atrioventricular conduction capacity were assessed before and every five minutes up to 30 minutes after intravenous administration of 0.15 mg of clonidine. The following significant maximal mean effects were noted at about 15 minutes after the administration of clonidine: the heart rate decreased 12 percent (59 vs 52 beats per minute); and the atrioventricular conduction capacity (ie, paced heart rate at second-degree atrioventricular block) decreased by 9 percent (132 vs 121 beats per minute), while the maximal recovery time of the sinus node increased by a factor of two (1,704 vs 3,562 msec) when atrial overdrives of 120, 150, and 200 beats per minute were used for each five minute period. In analyzing maximal carotid sinus pressure slowing after administration of clonidine, three of 11 patients developed hypersensitive carotid sinus reflex de novo, and two patients showed a decrease and three patients an increase of carotid sinus pressure slowing, while three patients had no carotid sinus pressure slowing both before and after administration of clonidine. We conclude that caution should be taken in administering clonidine to patients with signs indicative of dysfunction of the sinus node.
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PMID:Effects of clonidine on sinus node function in man. 701 48

Baroreceptor reflexes have been found to be attenuated during halothane anesthesia in humans and experimental animals. The baroreceptor reflex arc is comprised for a number of components, including receptors, afferent and efferent nerve pathways, central integratory centers, peripheral ganglia, and effector organs, at which halothane might exert an inhibitory effect. This study was performed to determine the effect of halothane at each component in order to identify the site or sites of baroreflex attenuation due to halothane. The baroreflex effects on heart rate initiated by carotid sinus pressure changes were examined in conscious and anesthetized (0.0%, 0.75%, and 1.5% halothane in 50% N2O and O2, pls 25 mg/kg thiopental) dogs. In addition, carotid sinus afferent activity, cardiac sympathetic efferent activity and heart responses to direct sympathetic and parasympathetic efferent stimulation were examined in anesthetized dogs. Preganglionic and postganglionic sympathetic nerve activities were recorded simultaneously during baroreceptor activation to determine ganglionic effects of halothane. All levels of anesthesia significantly (P less than 0.05) attenuated reflex changes in heart rate produced by the pressure changes compared to conscious dogs. Significant decreases in cardiac sympathetic efferent activity were produced at 1.5% halothane (P less than 0.05). The depression in postganglionic activity was significantly greater than that or preganglionic activity, indicating a ganglionic-blocking effect by halothane. Cardiac chronotropic changes produced by direct efferent stimulation of sympathetic and vagal fibers were attenuated significantly by halothane (P less than 0.05). On the other hand, baroreceptor afferent activity was increased at 1.5% halothane. This sensitization of baroreceptors appeared to contribute to decreased levels of sympathetic tone, leading to blunted reflex changes in nerve activity. Therefore, halothane was found to have multiple sites of action, leading to depression of the baroreflex.
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PMID:Halothane and the carotid sinus reflex: evidence for multiple sites of action. 711 41

The open-loop carotid sinus reflex control of systemic haemodynamics was studied in an acute dog preparation with isolated perfused carotid sinuses at three end-tidal halothane levels of 0.66 +/- 0.02% (HI); 0.88 +/- 0.02% (H2); and 1.17 +/- 0.02% (H3), in order to investigate the dose dependency of the carotid sinus reflex operating characteristics for halothane. Corresponding to the above halothane levels were reflex operating point pressures (set point pressures) of 104.9 +/- 2.9, 103.3 +/- 4.1 and 76.0 +/- 3.8 mmHg, respectively. Carotid sinus reflex gain decreased significantly with progressively increasing halothane levels (1.4. +/- 0.18; 0.84 +/- 0.12; 0.48 +/- 0.09), as did the range of reflex changes in systemic arterial pressure for equal overall changes in carotid sinus pressure (87.1 +/- 7.9; 64.1 +/- 7.4; 33.6 +/- 5.1 mmHg; P less than 0.01). For halothane levels below approximately 0.9%, this depression was not dependent upon changes in mean systemic arterial pressure. The relationship between reflex gain and halothane concentration could be described by a first-order exponential which suggested virtual ablation of the carotid sinus reflex control of mean arterial pressure at an end-tidal halothane concentration exceeding about 1.6%.
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PMID:Baroreceptor control of systemic haemodynamic at incremental halothane levels in the dog. 734 Mar 73

Arginine vasopressin (AVP) has profound effects on the cardiovascular system, yet has minimal pressor activity at physiological levels in intact subjects. We designed an investigation to delineate the effects of AVP on open-loop carotid baroreflex control of mean arterial pressure (MAP), total peripheral resistance (TPR), and cardiac output (CO) in conscious, chronically instrumented dogs. During graded infusions of AVP (0.5-2.0 ng.kg-1.min-1), the open-loop hemodynamic responses to controlled changes in isolated carotid sinus pressure (CSP) were determined. Increasing levels of AVP infusion led to significant increases in plasma AVP levels (P < 0.01). Increasing doses of AVP led to significant increases in TPR at all levels of CSP (P < 0.01). The overall range and gain of the response were not significantly different at any level of AVP infusion. Despite this increase in systemic resistance, there was no significant change in the MAP-CSP relationship. Infusion of AVP led to a dose-dependent depression in CO (P < 0.01) and heart rate (HR; P < 0.05) at all levels of CSP with no significant effect on open-loop baroreflex control. We conclude that although exogenous AVP induces profound changes in cardiovascular function, it does not alter carotid baroreflex control of MAP, TPR, CO, and HR.
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PMID:Exogenous arginine vasopressin does not enhance carotid baroreflex control in the conscious dog. 820 28

We tested the hypothesis that altering the pattern and/or magnitude of discharge of pulmonary stretch receptors (PSRs) would alter baroreceptor reflexes in anesthetized aortic-denervated cats. Carotid baroreceptor control of mean arterial pressure (MAP), heart rate (HR), and hindlimb perfusion pressure (PPhl) was examined by changing carotid sinus pressure (CSP) from 50 to 225 mmHg. The pattern of PSR discharge was changed by switching conventional mechanical ventilation (CMV) to high-frequency ventilation (HFV). Magnitude of PSR discharge was altered by changing positive end-expiratory pressure (PEEP). Altering the discharge pattern of PSR had no effect on CSP-MAP or CSP-PPhl relationships; small changes in HR were observed. Increasing PSR activity by increasing PEEP during CMV (from 3 to 9 cmH2O) depressed CSP-MAP relationship, set point, and threshold pressure. However, the depression in CSP-MAP relationship and set point during PEEP was unrelated to PSR activation, because these changes were not abolished after bilateral vagotomy. CSP-PPhl relationship was significantly elevated during PEEP before and after vagotomy, suggesting activation of a nonvagally mediated vasoconstrictory mechanism instead of PSR-mediated depressor reflex. CSP-HR relationship during PEEP showed a slight elevation, which was abolished after vagotomy. We conclude that despite minor increases in HR, altering the pattern of magnitude of PSR activity with HFV and PEEP has no significant effect on carotid baroreceptor regulation of systemic circulation. Hemodynamic changes observed during PEEP were likely due to its mechanical effect on cardiac output and activation of other cardiopulmonary receptors rather than to the increase in PSR activity.
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PMID:Effects of high-frequency ventilation and PEEP on carotid baroreceptor reflexes. 822 81


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