Sympathetic activation decreases medium-sized arterial compliance in humans

1994 ◽  
Vol 267 (4) ◽  
pp. H1368-H1376 ◽  
Author(s):  
P. Boutouyrie ◽  
P. Lacolley ◽  
X. Girerd ◽  
L. Beck ◽  
M. Safar ◽  
...  

This study used a precise noninvasive method in normotensive humans to determine the effects of sympathetic activation on arterial compliance. A recently developed, high-resolution echo-tracking system capable of measuring systolic/diastolic variations of arterial diameter was coupled to a Finapres system and used to calculate instantaneous systolic/diastolic pressure-diameter and compliance-pressure curves for a muscular medium-sized artery, the radial artery. Two standardized tests of sympathetic system activation, a cold pressor test (2 min) and a mental stress test (2 min of mental arithmetic), were performed at an interval of 8 days in random order in nine healthy volunteers [30 +/- 9 (SD) yr]. Radial arterial parameters were recorded every 30 s for 9 min, which included 2 min of cold pressor test or mental stress test. During both tests, radial arterial mean diameter did not change despite t he increase in mean arterial pressure (P < 0.001); stroke change in diameter decreased (P < 0.01), whereas pulse pressure increased (P < 0.01). Arterial compliance, calculated for the instantaneous level of mean arterial pressure, decreased significantly (P < 0.01). Compliance (C) calculated at 100 mmHg (C100) was arbitrarily chosen as a reference point for comparing compliance among the different periods of the test. C100 decreased significant (P < 0.05) during both tests (from 2.93 +/- 1.27 to 2.04 +/- 0.94 and from 3.29 +/- 1.73 to 2.63 +/- 1.55 mm2.mmHg-1.10(-3) during mental stress and the cold pressor test, respectively). These results indicate that sympathetic activation is able to decrease radial arterial compliance in healthy subjects. The reduction in arterial compliance probably resulted from complex interactions between changes in distending blood pressure and changes in radial arterial smooth muscle tone.

1990 ◽  
Vol 79 (1) ◽  
pp. 43-50 ◽  
Author(s):  
I. Marriott ◽  
Janice M. Marshall ◽  
E. J. Johns

1. Laser Doppler flowmetry has been used to study changes in cutaneous erythrocyte flux produced in the hand (i) on successive immersion of the contralateral hand in water at 20°C (cold test) and then in water at 0–4°C (cold pressor test), and (ii) by mental arithmetic. 2. In 11 subjects, placing the right hand in water at 20°C for 2 min induced a significant decrease in cutaneous erythrocyte flux in the contralateral hand and a significant fall in mean arterial pressure. Cutaneous vascular resistance, calculated as arterial pressure/cutaneous erythrocyte flux, showed no significant change. Thus, the decrease in erythrocyte flux was apparently due to a fall in perfusion pressure. 3. Subsequent immersion of the right hand in water at 0–4°C for 2 min caused a significant decrease in erythrocyte flux in the contralateral hand and a significant rise in mean arterial pressure. It is concluded that the cold pressor response evoked from one hand elicited a substantial reflex vasoconstriction in the skin of the other hand; accordingly, calculated cutaneous vascular resistance increased significantly. 4. Eight subjects performed mental arithmetic for two periods of 2 min separated by a rest period of 2 min. By the end of the second minute of each period of mental arithmetic there was a significant decrease in erythrocyte flux. Mean arterial pressure increased significantly in the first period only, but calculated cutaneous vascular resistance increased in both periods, consistent with cutaneous vasoconstriction. 5. The cold pressor test and mental arithmetic are aversive stimuli that evoke the characteristic pattern of the alerting or defence response which includes splanchnic vasoconstriction and muscle vasodilatation. Previous studies on the cutaneous vascular component of this response have yielded equivocal results. The present study provides firm evidence that it includes cutaneous vasoconstriction, at least in the hand.


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.


Author(s):  
Nasia Sheikh ◽  
Aaron A. Phillips ◽  
Shaun Ranada ◽  
Matthew Lloyd ◽  
Karolina Kogut ◽  
...  

Background: Initial orthostatic hypotension (IOH) is defined by a large drop in blood pressure (BP) within 15 s of standing. IOH often presents during an active stand, but not with a passive tilt, suggesting that a muscle activation reflex involving lower body muscles plays an important role. To our knowledge, there is no literature exploring how sympathetic activation affects IOH. We hypothesized involuntary muscle contractions before standing would significantly reduce the drop in BP seen in IOH while increasing sympathetic activity would not. Methods: Study participants performed 4 sit-to-stand maneuvers including a mental stress test (serial 7 mental arithmetic stress test), cold pressor test, electrical stimulation, and no intervention. Continuous heart rate and beat-to-beat BP were measured. Cardiac output and systemic vascular resistance were estimated from these waveforms. Data are presented as mean±SD. Results: A total of 23 female IOH participants (31±8 years) completed the study. The drops in systolic BP following the serial 7 mental arithmetic stress test (−26±12 mm Hg; P =0.004), cold pressor test (−20±15 mm Hg; P <0.001), and electrical stimulation (−28±12 mm Hg; P =0.01) were significantly reduced compared with no intervention (−34±11 mm Hg). The drops in systemic vascular resistance following the serial 7 mental arithmetic stress test (−391±206 dyne×s/cm 5 ; P =0.006) and cold pressor test (−386±179 dyne×s/cm 5 ; P =0.011) were significantly reduced compared with no intervention (−488±173 dyne×s/cm 5 ). Cardiac output was significantly increased upon standing (7±2 L/min) compared with during the sit (6±1 L/min; P <0.001) for electrical stimulation. Conclusion: Sympathetic activation mitigates the BP response in IOH, while involuntary muscle contraction mitigates the BP response and reduces symptoms. Active muscle contractions may induce both of these mechanisms of action in their pretreatment of IOH. Registration: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT03970551.


2020 ◽  
Vol 55 (2) ◽  
pp. 124-131 ◽  
Author(s):  
Blair D. Johnson ◽  
James R. Sackett ◽  
Zachary J. Schlader ◽  
John J. Leddy

Context Cardiovascular responses to the cold pressor test (CPT) provide information regarding sympathetic function. Objective To determine if recently concussed collegiate athletes had blunted cardiovascular responses during the CPT. Design Cross-sectional study. Setting Laboratory. Patients or Other Participants A total of 10 symptomatic concussed collegiate athletes (5 men, 5 women; age = 20 ± 2 years) who were within 7 days of diagnosis and 10 healthy control individuals (5 men, 5 women; age = 24 ± 4 years). Intervention(s) The participants' right hands were submerged in agitated ice water for 120 seconds (CPT). Main Outcome Measure(s) Heart rate and blood pressure were continuously measured and averaged at baseline and every 30 seconds during the CPT. Results Baseline heart rate and mean arterial pressure were not different between groups. Heart rate increased throughout 90 seconds of the CPT (peak increase at 60 seconds = 16 ± 13 beats/min; P &lt; .001) in healthy control participants but remained unchanged in concussed athletes (peak increase at 60 seconds = 7 ± 10 beats/min; P = .08). We observed no differences between groups for the heart rate response (P &gt; .28). Mean arterial pressure was elevated throughout the CPT starting at 30 seconds (5 ± 7 mm Hg; P = .048) in healthy control individuals (peak increase at 120 seconds = 26 ± 9 mm Hg; P &lt; .001). Mean arterial pressure increased in concussed athletes at 90 seconds (8 ± 8 mm Hg; P = .003) and 120 seconds (12 ± 8 mm Hg; P &lt; .001). Healthy control participants had a greater increase in mean arterial pressure starting at 60 seconds (P &lt; .001) and throughout the CPT than concussed athletes (peak difference at 90 seconds = 25 ± 10 mm Hg and 8 ± 8 mm Hg, respectively; P &lt; .001). Conclusions Recently concussed athletes had blunted cardiovascular responses to the CPT, which indicated sympathetic dysfunction.


1994 ◽  
Vol 16 (3) ◽  
pp. 163-167 ◽  
Author(s):  
Giuseppe Micieli ◽  
Cristina Tassorelli ◽  
Daniele Bosone ◽  
Anna Cavallini ◽  
Elena Viotti ◽  
...  

1999 ◽  
Vol 26 (10) ◽  
pp. 774-778 ◽  
Author(s):  
FRANCO LAGHI Pasini ◽  
PIER LEOPOLDO Capecchi ◽  
MARCELLA Colafati ◽  
PAOLA Randisi ◽  
LUCA Puccetti

2007 ◽  
Vol 5;10 (9;5) ◽  
pp. 677-685
Author(s):  
David M. Schultz

Background: Several animal studies support the contention that thoracic spinal cord stimulation (SCS) might decrease arterial blood pressure. Objective: To determine if electrical stimulation of the dorsal spinal cord in humans will lower mean arterial pressure (MAP) and heart rate (HR). Design: Case Series Methods: Ten normotensive subjects that were clinically indicated for SCS testing were studied. Two of the 10 patients who underwent testing were excluded from the analysis because they did not respond to the Cold Pressor Test (CPT). Systolic blood pressure, diastolic blood pressure, and heart rate were measured continuously at the wrist (using the Vasotrac device). SCS was administered with quadripolar leads implanted into the epidural space under fluoroscopic guidance. SCS was randomly performed either in the T1-T2 or T5-T6 region of the spinal cord during normal conditions as well as during transient stress induced by CPT. The CPT was conducted by immersing the non-dominant hand in ice-cold water for 2 minutes. Results: There were moderate decreases in MAP and HR during SCS at the T5-T6 region compared to baseline that did not reach statistical significance. However, SCS at the T1-T2 region tended to increase MAP and HR compared to baseline but the change did not reach statistical significance. Arterial blood pressure was transiently elevated by 9.4 ± 3.8 mmHg using CPT during the control period with SCS turned off and also during SCS at either the T1-T2 region or T5-T6 region of the spinal cord (by 9.2 ± 5 mmHg and 10.7 ± 8.4 mmHg, respectively). During SCS at T5-T6, the CPT significantly increased MAP by 5.9±7.1 mmHg compared to control CPT (SCS off). Conclusion: This study demonstrated that SCS at either the T1-T2 or T5-T6 region did not significantly alter MAP or HR compared to baseline (no SCS). However, during transcient stress (elevated sympathetic tone) induced by CPT, there was a significant increase in MAP and moderate decrease in HR during SCS at T5-T6 region, which is not consistent with previous data in the literature. Acute SCS did not result in adverse cardiovascular responses and proved to be safe. Key words: Spinal cord stimulation, mean arterial pressure, heart rate, cold pressor test


2011 ◽  
Vol 163 (1-2) ◽  
pp. 74
Author(s):  
M.J. Falvo ◽  
M. Blatt ◽  
J.J. Jasien ◽  
B.M. Deegan ◽  
G. OLaighin ◽  
...  

Author(s):  
Laura Marcela Reyes ◽  
Charlotte W. Usselman ◽  
Rshmi Khurana ◽  
Radha S. Chari ◽  
Michael K. Stickland ◽  
...  

Objective: To determine whether increased chemoreflex tonic activity is associated with augmented muscle sympathetic nervous sys activity (MSNA) in women diagnosed with preeclampsia. Methods: Women with preeclampsia (n=19; 32±5 years old, 31±3 weeks gestation) were matched by age and gestational age with pregnant women (controls, n=38, 32±4 years old, 31±4 weeks gestation; 2:1 ratio). MSNA (n=9 preeclampsia) was assessed during baseline, peripheral chemoreflex de-activation (hyperoxia) and a cold pressor test (CPT). Baroreflex gain, diastolic blood pressure at which there is a 50% likelihood of MSNA occurring (T50) and plasma noradrenaline concentrations were measured. Results: Baseline mean arterial pressure (MAP: 106±11 vs. 87±10 mmHg, p<0.0001), noradrenaline concentrations (498±152 pg/mL vs. 326±147, p=0.001) and T50 (79±7 vs. 71±9 mmHg, p=0.02) were greater in women with preeclampsia compared to controls. However, baseline MSNA (burst incidence [BI]: 41±16 vs. 45±13 bursts/100hb, p=0.4) was not different between groups. Responses to hyperoxia (ΔBI -5±7 vs. -1±8 bursts/100hb, p=0.1; ΔMAP -1±3 vs. -2±3 mmHg, p=0.7) and CPT (ΔBI 15±7 vs. 12±11 bursts/100hb, p=0.6; ΔMAP 10±4 vs. 12±11 mmHg, p=0.6) were not different between groups. Conclusion: Our findings question the assumption that increased MSNA contributes to hypertension in women with preeclampsia. The chemoreflex does not appear to contribute to an increase in MSNA in women with preeclampsia.


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