Cardiovascular and sympathoadrenal responses to mental stress: influence of beta-blockade

1988 ◽  
Vol 255 (6) ◽  
pp. H1443-H1451 ◽  
Author(s):  
U. Freyschuss ◽  
P. Hjemdahl ◽  
A. Juhlin-Dannfelt ◽  
B. Linde

Cardiovascular, sympathoadrenal, and subjective responses to mental stress induced by a color-word conflict test (CWT) were studied in 30 healthy males before and after intravenous administration of either placebo, beta 1-blockade by metoprolol (0.15 mg/kg), or nonselective beta-blockade by propranolol (0.15 mg/kg). CWT responses were reproducible. Mean arterial pressure increased by 20%. A mainly heart rate-dependent 65% increase in cardiac output (thermodilution) was associated with 25% decreases of both systemic (SVR) and calf vascular (CVR) resistances. Arterial plasma epinephrine (Epi) was doubled, and norepinephrine (NE) increased by 50%. Self-evaluated stress score correlated positively with changes in cardiac output and inversely with changes in SVR during CWT. Both metoprolol and propranolol halved heart rate responses; whereas increases in mean arterial pressure, Epi, and NE were uninfluenced. Metoprolol reduced the increase in stroke volume, and propranolol abolished it. SVR and CVR responses were attenuated by metoprolol and abolished by propranolol. The results suggest that mental stress accelerates the heart through neurogenic mechanisms and that peripheral vasodilatation is achieved through the concerted actions of reduced vasoconstrictor activity and elevated circulating Epi.

2004 ◽  
Vol 287 (5) ◽  
pp. H2309-H2315 ◽  
Author(s):  
Madeleine Lindqvist ◽  
Anders Melcher ◽  
Paul Hjemdahl

Cardiovascular and sympathoadrenal responses to a reproducible mental stress test were investigated in eight healthy young men before and during intravenous infusion of the nitric oxide (NO) synthesis inhibitor N-monomethyl-l-arginine (l-NMMA). Before l-NMMA, stress responses included significant increases in heart rate, mean arterial pressure, and cardiac output (CO) and decreases in systemic and forearm vascular resistance. Arterial plasma norepinephrine (NE) increased. At rest after 30 min of infusion of l-NMMA (0.3 mg·kg−1·min−1 iv), mean arterial pressure increased from 98 ± 4 to 108 ± 3 mmHg ( P < 0.001) because of an increase in systemic vascular resistance from 12.9 ± 0.5 to 18.5 ± 0.9 units ( P < 0.001). CO decreased from 7.7 ± 0.4 to 5.9 ± 0.3 l/min ( P < 0.01). Arterial plasma NE decreased from 2.08 ± 0.16 to 1.47 ± 0.14 nmol/l. Repeated mental stress during continued infusion of l-NMMA (0.15 mg·kg−1·min−1) induced qualitatively similar cardiovascular responses, but there was a marked attenuation of the increase in mean arterial blood pressure, resulting in similar “steady-state” blood pressures during mental stress without and with NO blockade. Increases in heart rate and CO were attenuated, but stress-induced decreases in systemic and forearm vascular resistance were essentially unchanged. Arterial plasma NE increased less than during the first stress test. Thus the increased arterial tone at rest during l-NMMA infusion is compensated for by attenuated increases in blood pressure during mental stress, mainly through a markedly attenuated CO response and suppressed sympathetic nerve activity.


1978 ◽  
Vol 55 (s4) ◽  
pp. 329s-332s ◽  
Author(s):  
A. J. Man in 't Veld ◽  
G. J. Wenting ◽  
R. P. Verhoeven ◽  
M. A. D. H. Schalekamp

1. Haemodynamic responses to diazoxide (300 mg intravenously) were studied in 15 hypertensive patients before and after chronic β-adrenoreceptor blockade by 320 mg of propranolol daily. After diazoxide alone, mean arterial pressure and total peripheral resistance were lowered by 24 ± 3 and 35 ± 5% (mean ± sem) respectively. Cardiac output and heart rate rose by 25 ± 9 and 21 ± 3%. During β-adrenoreceptor blockade, the percentage changes of mean arterial pressure, heart rate, cardiac output and total peripheral resistance after vasodilatation were not significantly different from those after diazoxide alone. 2. Atropine, 0·04 mg/kg body weight, was given to 12 hypertensive patients chronically treated with β-adrenoreceptor blockade, before acute vasodilatation by diazoxide. Diazoxide caused no increase in heart rate after combined β-adrenoreceptor and parasympathetic blockade. However, cardiac output rose by 14 ± 5%. 3. We conclude that withdrawal of parasympathetic tone is an important determinant of circulatory homeostasis after acute vasodilatation during β-adrenoreceptor blockade.


1988 ◽  
Vol 74 (3) ◽  
pp. 293-299 ◽  
Author(s):  
Jean-Francois Liard

1. The specific antidiuretic agonist [4-valine, 8-d-arginine]vasopressin (VDAVP) was administered intravenously to seven conscious dogs at a rate of 10 ng min−1 kg−1. Cardiac output (aortic electromagnetic flowmeter), mean arterial pressure and regional blood flows (radioactive microspheres) were measured before and after 30 min of infusion. 2. Mean arterial pressure fell from 89.9 ± 4.5 (mean ± sem) to 82.3 ± 5.9 mmHg and cardiac output increased from 115.4 ± 8.7 to 163.0 ± 14.4 ml min−1 kg−1. Total peripheral resistance decreased from 41.6 ± 3.7 to 27.8 ± 3.6 units and heart rate increased from 79.2 ± 5.9 to 123.2 ± 5.9 beats/min. Blood flow increased significantly in the myocardium, fat and skeletal muscle vascular bed. 3. In another group of six dogs subjected to a similar protocol 24 h after bilateral nephrectomy, mean arterial pressure fell from 102.2 ± 5.3 to 82.7 ± 3.4 mmHg and cardiac output increased from 125.6 ± 3.0 to 171.2 ± 4.0 ml min−1 kg−1. Total peripheral resistance decreased from 39.3 ± 3.4 to 23.4 ± 1.3 units and heart rate increased from 84 ± 4.9 to 113.3 ± 4.3 beats/min. The increase in cardiac output and the fall in total peripheral resistance did not differ significantly between intact and anephric dogs. Regional blood flow responses differed in some respects in the two groups studied, but there was no evidence that the vasodilatory action of VDAVP depended on the presence of the kidneys. 4. These results indicate that the vasodilatation elicited by the antidiuretic agonist VDAVP in intact dogs is limited to a few vascular beds. Furthermore, this vasodilatation appears to be independent from the renal V2-vasopressin receptors.


2017 ◽  
Vol 26 (1) ◽  
pp. 31-36 ◽  
Author(s):  
Rosario Arcaya Nievera ◽  
Ann Fick ◽  
Hilary K. Harris

Purpose To assess the safety of mobilizing patients receiving low-dose norepinephrine (0.05 μg/kg per min) by examining mean arterial pressure and heart rate before and after activity with parameters set by the physician. Background Norepinephrine is a peripheral vasoconstrictor administered for acute hypotension. During activity, blood flows to the periphery to supply muscles with oxygen, which may oppose the norepinephrine vasoconstriction. The safety of mobilizing patients receiving norepinephrine is unclear. Methods Heart rate, mean arterial pressure, norepinephrine dose, and activity performed were extracted retrospectively from charts of 47 cardiothoracic surgery patients during the first patient transfer to chair or ambulation with norepinephrine infusing. Mean arterial pressure and heart rate were compared before and after physical therapy (paired t tests). Differences among norepinephrine doses and physical activity levels were evaluated (Kruskal-Wallis test). Results Forty-one of the 47 patients (87%) tolerated the activity within safe ranges of vital signs. The change in patients’ mean arterial pressure from before to after activity was not significant (P = .16), but a significant increase in heart rate occurred after activity (P &lt; .001). A Kruskal-Wallis test showed no significant difference in the norepinephrine dose and activity level (χ2 = 6.34, P = .17). No instances of cardiopulmonary or respiratory arrest occurred during any physical therapy sessions. Conclusions Infusion of low-dose norepinephrine should not be considered an automatic reason to keep patients on bed rest.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Jérémy Cros ◽  
Lucie Bidlingmeyer ◽  
Robin Rosset ◽  
Kevin Seyssel ◽  
Camille Crézé ◽  
...  

Abstract Background The mechanisms by which chronic stress increases the risk of non-communicable diseases remain poorly understood. On one hand, chronic stress may increase systemic vascular resistance (SVR) and blood pressure, which may lead to blood vessels injury and altered myocardial perfusion. On the other hand, chronic stress may promote the overconsumption of sugar-containing foods and favor obesity. There is indeed evidence that sweet foods are preferentially consumed to alleviate stress responses. The effects of nutritive and non-nutritive sweeteners (NNS) on hemodynamic stress responses remain however largely unknown. Objective/design This study aimed at comparing the effects of sucrose-containing and NNS-containing drinks, as compared to unsweetened water, on hemodynamic responses to acute stress in twelve healthy female subjects. Acute stress responses were elicited by a 30-min mental stress (5-min Stroop’s test alternated with 5-min mental arithmetic) and a 3-min cold pressure test (CPT), each preceded by a resting baseline period. Hemodynamic stress responses were investigated by the repeated measurement of mean arterial pressure and the continuous monitoring of cardiac output by thoracic electrical bioimpedance measurement. SVR was selected as a primary outcome because it is a sensitive measure of hemodynamic responses to acute stress procedures. Results With all three drinks, SVR were not changed with mental stress (P = 0.437), but were increased with CPT (P = 0.045). Both mental stress and CPT increased mean arterial pressure and heart rate (all P < 0.001). Cardiac output increased with mental stress (P < 0.001) and remained unchanged with CPT (P = 0.252). No significant differences in hemodynamic responses were observed between water, sucrose and NNS (stress × condition, all P > 0.05). Conclusions These results demonstrate that sucrose and NNS do not alter hemodynamic responses to two different standardized acute stress protocols.


2001 ◽  
Vol 280 (5) ◽  
pp. R1462-R1468 ◽  
Author(s):  
Holly R. Middlekauff ◽  
Jun Liang Yu ◽  
Kakit Hui

In animal studies, acupuncture has been shown to be sympathoinhibitory, but it is unknown if acupuncture is sympathoinhibitory in humans. Nineteen healthy volunteers underwent mental stress testing pre- and postacupuncture. Muscle sympathetic nerve activity (MSNA), blood pressure, and heart rate during mental stress were compared pre- and postacupuncture. Control acupuncture consisted of acupuncture at nonacupoints and “no-needle” acupuncture. Acupuncture had no effect on resting MSNA, blood pressure, or heart rate. After real acupuncture, the increase in mean arterial pressure (pre- vs. postacupuncture 4.5 vs. 1.7 mmHg, P < 0.001), but not MSNA or heart rate, was blunted during mental stress. Similarly, following nonacupoint acupuncture, the increase in mean arterial pressure was blunted during mental stress (5.4 vs. 2.9 mmHg, P < 0.0003). No-needle acupuncture had no effect on these variables. In conclusion, acupuncture at traditional acupoints, nonacupoints, and no-needle acupuncture does not modulate baseline MSNA or MSNA responses to mental stress in normal humans. Acupuncture significantly attenuates the increase in blood pressure during mental stress. Needling nonacupoints, but not “no-needle” acupuncture, have a similar effect on blood pressure.


2000 ◽  
Vol 93 (2) ◽  
pp. 382-394 ◽  
Author(s):  
Thomas J. Ebert ◽  
Judith E. Hall ◽  
Jill A. Barney ◽  
Toni D. Uhrich ◽  
Maelynn D. Colinco

Background This study determined the responses to increasing plasma concentrations of dexmedetomidine in humans. Methods Ten healthy men (20-27 yr) provided informed consent and were monitored (underwent electrocardiography, measured arterial, central venous [CVP] and pulmonary artery [PAP] pressures, cardiac output, oxygen saturation, end-tidal carbon dioxide [ETCO2], respiration, blood gas, and catecholamines). Hemodynamic measurements, blood sampling, and psychometric, cold pressor, and baroreflex tests were performed at rest and during sequential 40-min intravenous target infusions of dexmedetomidine (0.5, 0.8, 1.2, 2.0, 3.2, 5.0, and 8.0 ng/ml; baroreflex testing only at 0.5 and 0.8 ng/ml). Results The initial dose of dexmedetomidine decreased catecholamines 45-76% and eliminated the norepinephrine increase that was seen during the cold pressor test. Catecholamine suppression persisted in subsequent infusions. The first two doses of dexmedetomidine increased sedation 38 and 65%, and lowered mean arterial pressure by 13%, but did not change central venous pressure or pulmonary artery pressure. Subsequent higher doses increased sedation, all pressures, and calculated vascular resistance, and resulted in significant decreases in heart rate, cardiac output, and stroke volume. Recall and recognition decreased at a dose of more than 0.7 ng/ml. The pain rating and mean arterial pressure increase to cold pressor test progressively diminished as the dexmedetomidine dose increased. The baroreflex heart rate slowing as a result of phenylephrine challenge was potentiated at both doses of dexmedetomidine. Respiratory variables were minimally changed during infusions, whereas acid-base was unchanged. Conclusions Increasing concentrations of dexmedetomidine in humans resulted in progressive increases in sedation and analgesia, decreases in heart rate, cardiac output, and memory. A biphasic (low, then high) dose-response relation for mean arterial pressure, pulmonary arterial pressure, and vascular resistances, and an attenuation of the cold pressor response also were observed.


2008 ◽  
Vol 108 (5) ◽  
pp. 802-811 ◽  
Author(s):  
Robert A. Dyer ◽  
Jenna L. Piercy ◽  
Anthony R. Reed ◽  
Carl J. Lombard ◽  
Leann K. Schoeman ◽  
...  

Background Hemodynamic responses to spinal anesthesia (SA) for cesarean delivery in patients with severe preeclampsia are poorly understood. This study used a beat-by-beat monitor of cardiac output (CO) to characterize the response to SA. The hypothesis was that CO would decrease from baseline values by less than 20%. Methods Fifteen patients with severe preeclampsia consented to an observational study. The monitor employed used pulse wave form analysis to estimate nominal stroke volume. Calibration was by lithium dilution. CO and systemic vascular resistance were derived from the measured stroke volume, heart rate, and mean arterial pressure. In addition, the hemodynamic effects of phenylephrine, the response to delivery and oxytocin, and hemodynamics during recovery from SA were recorded. Hemodynamic values were averaged for defined time intervals before, during, and after SA. Results Cardiac output remained stable from induction of SA until the time of request for analgesia. Mean arterial pressure and systemic vascular resistance decreased significantly from the time of adoption of the supine position until the end of surgery. After oxytocin administration, systemic vascular resistance decreased and heart rate and CO increased. Phenylephrine, 50 mug, increased mean arterial pressure to above target values and did not significantly change CO. At the time of recovery from SA, there were no clinically relevant changes from baseline hemodynamic values. Conclusions Spinal anesthesia in severe preeclampsia was associated with clinically insignificant changes in CO. Phenylephrine restored mean arterial pressure but did not increase maternal CO. Oxytocin caused transient marked hypotension, tachycardia, and increases in CO.


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.


Sign in / Sign up

Export Citation Format

Share Document