Hemodynamic and respiratory responses to carotid sinus pressure alteration in experimental hypertension

1993 ◽  
Vol 74 (3) ◽  
pp. 1274-1279 ◽  
Author(s):  
M. J. Brunner ◽  
M. D. Kligman

The purpose of this study was to determine whether baroreflex control of respiratory responses is diminished in hypertension. Ten dogs were made chronically hypertensive with use of a bilateral renal wrap technique. Eight sham-operated dogs served as normotensive controls. After the development of experimental hypertension, carotid baroreflex control of arterial pressure, heart rate, respiratory frequency, tidal volume, and ventilation was acutely assessed. Under pentobarbital anesthesia and with bilateral vagotomy, the carotid sinuses were isolated and perfused at controlled pressures. Before the carotid sinus region was manipulated, the mean arterial pressure was significantly higher (P < 0.005) in the hypertensive group (146.4 +/- 2.3 mmHg) than in the normotensive group (124.7 +/- 2.6 mmHg). The mean arterial pressures and heart rates measured at every level of carotid sinus pressure were significantly higher in the hypertensive group. Reflex gain of heart rate, but not mean arterial pressure, was significantly reduced in the hypertensive group. Respiratory frequency, tidal volume, and ventilatory responses to changes in carotid sinus pressure were significant and resulted in an approximately 40% reflex change in ventilation. These responses were not diminished in the hypertensive group. We conclude that respiratory baroreflex responses are preserved in experimental hypertension.

1992 ◽  
Vol 262 (5) ◽  
pp. H1508-H1514
Author(s):  
M. J. Brunner ◽  
M. D. Kligman

The hypothesis tested was that the rapid resetting of the arterial baroreflex control of arterial pressure in normotension could be demonstrated in experimental hypertension. After the development of experimental hypertension (using a bilateral renal wrap technique), rapid resetting of arterial pressure and heart rate (HR) was acutely assessed under pentobarbital sodium anesthesia in hypertensive and normotensive vagotomized dogs. The carotid sinus area was isolated and perfused at controlled carotid sinus pressures (CSPs). Baroreflex response [mean arterial pressure (MAP) and HR] curves were measured after three carotid sinus conditioning pressures (50, 125, and 200 mmHg) were applied. For the MAP response, the CSPo (CSP at point of maximum reflex gain) increased significantly to the same extent in both groups with increasing conditioning pressures (with 22.2 and 16.7% resetting in the normotensive group, and 20.3 and 14.2% resetting in the hypertensive group). We conclude that short-term adjustments to changes in prevailing pressure (rapid resetting) occur in the arterial pressure response in experimental hypertension to the same extent seen in normotension.


1993 ◽  
Vol 265 (3) ◽  
pp. H986-H992
Author(s):  
M. J. Brunner ◽  
G. G. Bishop ◽  
K. Shigemi ◽  
J. P. Freeman ◽  
D. Chung

The effect of the carotid sinus baroreflex reflex on arterial pressure-flow relationships was studied in Goldblatt hypertensive and normotensive dogs on cardiopulmonary bypass. Dogs were anesthetized with pentobarbital sodium, vagotomized, and the carotid sinuses were isolated at controlled carotid sinus pressures (CSP). The mean arterial pressure-flow relationships were measured at different levels of CSP. The arterial pressure-flow relationship was found to be linear except at extreme levels of flow. The slopes derived from the linear regression of the pressure-flow relationships [total peripheral resistance (TPR)] were 1.466 +/- 0.111 and 0.786 +/- 0.13 mmHg.ml-1 x min.kg at CSP of 50 and 200 mmHg in the normotensive group and 1.758 +/- 0.183 and 0.937 +/- 0.114 mmHg.ml-1 x min.kg at CSP of 50 and 250 mmHg in the hypertensive group. The increases in slope measured when CSP was decreased from saturation to threshold were 0.68 mmHg.ml-1 x min.kg (187% increase) in the normotensive group and 0.82 mmHg.ml-1 x min.kg (188% increase) in the hypertensive group. Zero-flow arterial pressures at CSP of 50, 125, and 200 mmHg were found to be 23.1 +/- 2.9, 21.7 +/- 2.2, and 17.1 +/- 1.8 mmHg in the normotensive group and 28.4 +/- 2.2, 23.8 +/- 1.5, and 20.0 +/- 1.2 mmHg in the hypertensive group. A nonlinear model fit was found to give a significantly better fit [coefficient of determination (r2) = 0.932 linear, 0.956 nonlinear] of the arterial pressure-flow relationships. We conclude that, in experimental hypertension, carotid baroreflex control of TPR is shifted to a higher operating point without any reduction in overall reflex gain.


1987 ◽  
Vol 252 (2) ◽  
pp. R294-R298 ◽  
Author(s):  
V. S. Bishop ◽  
R. E. Shade ◽  
J. R. Haywood ◽  
C. Hamm

There is considerable controversy as to whether removal of baroreceptor input by sinoaortic deafferentation leads to a sustained hypertension in quadripeds. Because of the importance of the baroreflex during postural changes, the effects of baroreceptor denervation may be even more profound in the primate. In this study, six adult male baboons (Papio anubis) were maintained on a tether system to examine the acute and sustained effects of aortic and combined carotid sinus and aortic baroreceptor deafferentation. Mean arterial pressure (MAP) averaged over 24 h increased from 86 +/- 4.0 to 105 +/- 5.5 mmHg after aortic denervation. One week after sinoaortic deafferentation, arterial pressure rose to 129 +/- 12.9 mmHg and then receded to 97 +/- 4.4 mmHg at 4 wk postdenervation. The lability of arterial pressure (measured as the mean of the standard deviations over 24 h) did not change with aortic denervation but increased at 1 and 4 wk after complete baroreceptor denervation. These studies indicate that baroreceptor deafferentation in the primate results in an acute increase in arterial pressure, the lability of arterial pressure, and heart rate. However, by 4 wk postdenervation, the level and lability of arterial pressure are decreased but remain significantly elevated.


2018 ◽  
Vol 596 (8) ◽  
pp. 1373-1384 ◽  
Author(s):  
Thomas J. Hureau ◽  
Joshua C. Weavil ◽  
Taylor S. Thurston ◽  
Ryan M. Broxterman ◽  
Ashley D. Nelson ◽  
...  

1984 ◽  
Vol 66 (1) ◽  
pp. 17-25 ◽  
Author(s):  
Robert Fagard ◽  
Anne Cattaert ◽  
Paul Lijnen ◽  
Jan Staessen ◽  
Luc Vanhees ◽  
...  

1. The systemic circulation at rest and during exercise was studied in ten normal male volunteers, after placebo on one occasion and after acute intravenous administration of the serotonergic antagonist ketanserin on another occasion. The effects of ketanserin on the components of the renin—angiotensin—aldosterone system, on plasma catecholamines and on exercise capacity for graded uninterrupted exercise were also investigated. 2. At rest in recumbency rapid intravenous injection of 10 mg of ketanserin, followed by a continuous infusion of 2 mg/h, produced an acute but transient fall in mean intra-arterial pressure of 6 mmHg compared with placebo. After 15 min the mean arterial pressure with ketanserin was within 2 mmHg of the mean pressure with placebo. In the sitting position both at rest and up to 30% of maximal work rate, the mean arterial pressure during ketanserin did not differ from the pressure on placebo. However, at higher levels of physical activity the rise in mean arterial pressure was lower with ketanserin; the pressure achieved with placebo was 7.5 mmHg higher at maximal work rate. Heart rate and cardiac output were significantly higher during ketanserin. 3. When the subjects were lying down and resting, plasma noradrenaline and adrenaline levels, plasma renin activity and angiotensin II concentration were not affected by ketanserin; however, these values were higher in the sitting position both at rest and during exercise. Plasma aldosterone was reduced by ketanserin during exercise and also when the subject was resting in the recumbent position. 4. Exercise capacity as measured by peak oxygen uptake was similar during ketanserin (3.09 ± se 0.12 litres/min) and during placebo (3.11 ± 0.13). 5. The data suggest that 5-hydroxytryptamine can have only a small role, if any, in pressure homoeostasis in sodium replete man at rest in recumbency. At moderate and heavy levels of exercise, the results are compatible with a role for 5-hydroxytryptamine in pressure regulation. Activation of the sympathetic nervous system by ketanserin is suggested by increases of plasma catecholamines, heart rate, cardiac output and plasma renin. The suppression of plasma aldosterone suggests that 5-hydroxytryptamine may have a role in the regulation of aldosterone secretion which is independent of angiotensin II.


2021 ◽  
pp. 90-95
Author(s):  
O. L. Tkachuk ◽  
R. L. Parakhoniak ◽  
S. V. Melnyk ◽  
O. O. Tkachuk-Hryhorchuk

Pneumoperitoneum is one of the most critical components of laparoscopic surgery, which has a negative effect on gas exchange and stress to circulatory buffering system. One of the top priorities of laparoscopic technologies is to minimize the impact on the respiratory and cardiovascular systems, metabolic dynamics and compensatory abilities of homeostasis. The main goal of this research work is to compare the effects of carboxyperitoneum and argonoperitoneum on the intraoperative dynamics of CO2 concentration as well as cardiovascular and respiratory characteristics in patients undergoing laparoscopic cholecystectomy for various forms of cholelithiasis. Materials and methods. Four experimental groups involved patients based on their nosological form of cholelithiasis and the gas used to induce pneumoperitoneum. All patients underwent laparoscopic cholecystectomy by means of standard procedure. Either medical carbon dioxide or medical argon was used to induce pneumoperitoneum. Intraoperative monitoring of blood carbon dioxide levels PaCO2 was performed by taking venous blood every 15 minutes. Capnometry was performed by means of mainstream analysis using “BIOMED” BM1000C modular patient monitor by recording the discrete values of PetCO2 every 15 minutes, as well as by analyzing photocopies of capnography curves every 15 minutes. Intraoperative echocardiography was performed to identify the mean arterial pressure (MAP), heart rate (HR) and cardiac output (CO) in order to assess the effects of different types of pneumoperitoneum on the cardiovascular system. Results. The obtained data confirm the expected difference in the indices of cardiorespiratory functions between patients with acute cholecystitis and cholelithiasis without signs of inflammation. The investigation revealed that under the influence of pneumoperitoneum, heart rate and mean arterial pressure increase, while the cardiac output decreases. The respiratory pressure marker depends more on the intra-abdominal pressure and presumably the patient’s body type than on the presence of inflammatory syndrome. Argon insufflation has a slight negative impact on the cardiovascular system. Particularly, the mean arterial pressure and heart rate increase, while the cardiac output marker is less decreased as compared to the use of carbon dioxide. Abdominal pressure has a significant effect on the cardiovascular and respiratory systems regardless of the used type of gas. The combination of high intra-abdominal pressure with the elevated head end of the operating table, which is a common practise during cholecystectomy, has especially great influence on cardiovascular and respiratory functions. Operation which is carried out at decreased pressure allows reducing the deviations of practically all indices. Conclusions. Thus, the cardiovascular and respiratory systems adapt under the influence of pneumoperitoneum, providing compensation for the negative effects of mechanical and resorptive-metabolic character. Compensatory-adaptive abilities of the cardiovascular and respiratory systems increase with the decrease of intra-abdominal pressure. The use of argon as a working gas for insufflation into the abdominal cavity during laparoscopy reduces the negative impact of pneumoperitoneum on the cardiovascular and respiratory systems, providing a greater reserve of homeostatic and buffer systems of the body.


1986 ◽  
Vol 61 (2) ◽  
pp. 797-803 ◽  
Author(s):  
T. J. Ebert

The simultaneous rise in heart rate and arterial pressure during isometric handgrip exercise suggests that arterial baroreflex control may be altered. We applied incremental intensities of neck suction and pressure to nine healthy young men to alter carotid sinus transmural pressure. Carotid stimuli were delivered during 1) supine control, 2) “anticipation” of beginning exercise, and 3) handgrip (20% of maximum voluntary contraction). Anticipation was a quiet period, immediately preceding the beginning of handgrip, when no muscular work was being performed. Compared with control, the R-R interval prolongation and mean arterial pressure decline provoked by carotid stimuli were decreased during the anticipation period. These data suggest that influences from higher central neural locations may alter baroreflex function. Furthermore, we derived stimulus-response curves relating carotid sinus transmural pressure to changes in R-R interval and mean arterial pressure. These curves were shifted during handgrip; however, calculated regression slopes were not changed from control. The data indicate that isometric handgrip exercise has a specific influence on human carotid baroreflex control of arterial pressure and heart period: baroreflex function curves are shifted rightward during handgrip, whereas baroreflex sensitivity is unchanged. Furthermore, central neural influences may be partially involved in these alterations.


1987 ◽  
Vol 253 (6) ◽  
pp. H1409-H1417 ◽  
Author(s):  
M. Miki ◽  
K. Miki ◽  
G. Hajduczok ◽  
D. Curran-Everett ◽  
J. A. Krasney

The contribution of the sinoaortic reflexes to the control of both the mean level and variability of arterial pressure (Pa) and heart rate (HR) was studied in five adult ewes after chronic section of the carotid sinus and aortic depressor nerves (SAD). SAD group responses were compared with a sham-operated group (n = 6). Pa was 15% lower in the SAD group due to a reduction of total peripheral resistance. The standard deviations and coefficients of variation for both Pa and HR obtained by continuous 16-h monitoring (10-s intervals) in the SAD sheep were not significantly different from those of the sham group. Arterial hypoxia (arterial PO2 = 40 mmHg for 96 h) had no significant influence on the mean values or variability for Pa and HR for either group, although both groups spent more time lying down. Ventilation was unchanged in the SAD group. Thus mean Pa is lower after removal of baroreceptor and chemoreceptor inputs, but the variabilities of both HR and Pa are unaltered during both normoxia and hypoxia in this sedentary species.


1988 ◽  
Vol 254 (6) ◽  
pp. R1025-R1034
Author(s):  
R. A. Shammas ◽  
A. L. Denison ◽  
T. W. Pfennig ◽  
D. P. Hemker ◽  
R. B. Stephenson

Previous studies showed that baroreflex control of heart rate is impaired during operant shock avoidance conditioning and classical aversive conditioning. However, the effects of such "emotionally stressful" paradigms on the ability of the baroreflex to control arterial pressure have not been directly assessed. We prepared the carotid sinus regions of dogs for reversible isolation from the systemic circulation, and we derived complete stimulus-response relations for the effects of carotid sinus pressure on both heart rate and arterial pressure. For any given carotid sinus pressure, arterial pressure and heart rate were higher during operant shock-avoidance conditioning and during classical aversive conditioning than in a neutral environment, which indicates an upward resetting of the baroreflex. However, threshold and saturation carotid sinus pressures were unaffected by operant conditioning or classical conditioning, which indicates that the baroreceptors themselves were not reset. The ranges over which the carotid baroreflex could vary arterial pressure and heart rate were significantly increased during both operant conditioning and classical conditioning. Baroreflex gain was unchanged during operant conditioning and was significantly increased during classical conditioning. We conclude that the baroreflex is not impaired during operant shock-avoidance conditioning or classical aversive conditioning in dogs. However, the baroreflex is reset and regulates blood pressure at an elevated level.


2000 ◽  
Vol 88 (3) ◽  
pp. 957-965 ◽  
Author(s):  
Jacqui Raymond ◽  
Glen M. Davis ◽  
Martinus N. van der Plas ◽  
Herbert Groeller ◽  
Scott Simcox

This study investigated control of heart rate (HR) and mean arterial pressure (MAP) at rest and during electrical stimulation (ES) leg cycling exercise (LCE) in paraplegics (Para). Seven men with complete spinal lesions (T5–T11) and six able-bodied (AB) men participated in this study. Beat-to-beat changes in HR and MAP were recorded during carotid sinus perturbation. Carotid baroreflex function curves were derived at rest and during ES-LCE for Para and during voluntary cycling (Vol) for AB. From rest to ES-LCE, oxygen uptake (V˙o 2) increased (by 0.43 l/min) and HR rose (by 11 beats/min), yet MAP remained unchanged. In AB, Vol increased V˙o 2 (by 0.53 l/min), HR (by 22 beats/min), and MAP (by 8 mmHg). ES-LCE did not alter the carotid sinus pressure (CSP)-MAP relationship, but it displaced the CSP-HR relationship upward relative to rest. No rightward shift was observed during ES-LCE. Vol by AB produced an upward and rightward displacement of the CSP-MAP and CSP-HR relationships relative to rest. These findings suggested that the carotid sinus baroreflex was not reset during ES-LCE in Para.


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