scholarly journals Heat stress attenuates the increase in arterial blood pressure during the cold pressor test

2010 ◽  
Vol 109 (5) ◽  
pp. 1354-1359 ◽  
Author(s):  
Jian Cui ◽  
Manabu Shibasaki ◽  
David A. Low ◽  
David M. Keller ◽  
Scott L. Davis ◽  
...  

The mechanisms by which heat stress impairs the control of blood pressure leading to compromised orthostatic tolerance are not thoroughly understood. A possible mechanism may be an attenuated blood pressure response to a given increase in sympathetic activity. This study tested the hypothesis that whole body heating attenuates the blood pressure response to a non-baroreflex-mediated sympathoexcitatory stimulus. Ten healthy subjects were instrumented for the measurement of integrated muscle sympathetic nerve activity (MSNA), mean arterial blood pressure (MAP), heart rate, sweat rate, and forearm skin blood flow. Subjects were exposed to a cold pressor test (CPT) by immersing a hand in an ice water slurry for 3 min while otherwise normothermic and while heat stressed (i.e., increase core temperature ∼0.7°C via water-perfused suit). Mean responses from the final minute of the CPT were evaluated. In both thermal conditions CPT induced significant increases in MSNA and MAP without altering heart rate. Although the increase in MSNA to the CPT was similar between thermal conditions (normothermia: Δ14.0 ± 2.6; heat stress: Δ19.1 ± 2.6 bursts/min; P = 0.09), the accompanying increase in MAP was attenuated when subjects were heat stressed (normothermia: Δ25.6 ± 2.3, heat stress: Δ13.4 ± 3.0 mmHg; P < 0.001). The results demonstrate that heat stress can attenuate the pressor response to a sympathoexcitatory stimulus.

1993 ◽  
Vol 3 (5) ◽  
pp. 303-310 ◽  
Author(s):  
Frank Weise ◽  
Dominique Laude ◽  
Arlette Girard ◽  
Philippe Zitoun ◽  
Jean-Philippe Siché ◽  
...  

2007 ◽  
Vol 21 (5) ◽  
Author(s):  
Jian Cui ◽  
Manabu Shibasaki ◽  
David Low ◽  
David Keller ◽  
Scott Davis ◽  
...  

1985 ◽  
Vol 69 (5) ◽  
pp. 533-540 ◽  
Author(s):  
Gianfranco Parati ◽  
Guido Pomidossi ◽  
Agustin Ramirez ◽  
Bruno Cesana ◽  
Giuseppe Mancia

1. In man evaluation of neural cardiovascular regulation makes use of a variety of tests which address the excitatory and reflex inhibitory neural influences that control circulation. Because interpretation of these tests is largely based on the magnitude of the elicited haemodynamic responses, their reproducibility in any given subject is critical. 2. In 39 subjects with continuous blood pressure (intra-arterial catheter) and heart rate monitoring we measured (i) the blood pressure and heart rate rises during hand-grip and cold-pressor test, (ii) the heart rate changes occurring during baroreceptor stimulation and deactivation by injection of phenylephrine and trinitroglycerine, and (iii) the heart rate and blood pressure changes occurring with alteration in carotid baroreceptor activity by a neck chamber. Each test was carefully standardized and performed at 30 min intervals for a total of six times in each subject. 3. The results showed that the responses to any test were clearly different from one another and that this occurred in all subjects studied. For the group as a whole the average response variability (coefficient of variation) ranged from 10.2% for the blood pressure response to carotid baroreceptor stimulation to 44.2% for the heart rate response to cold-pressor test. The variability of the responses was not related to basal blood pressure or heart rate, nor to the temporal sequence of the test performance. 4. Thus tests employed for studying neural cardiovascular control in man produce responses whose reproducibility is limited. This phenomenon may make it more difficult to define the response magnitude typical of each subject, as well as its comparison in different conditions and diseases.


1994 ◽  
Vol 72 (10) ◽  
pp. 1193-1199 ◽  
Author(s):  
R. D. Kilgour ◽  
J. Carvalho

To test the hypothesis that changes in systemic vascular resistance (SVR) contribute to the differences in arterial blood pressure responses between men and women to local cold pressor tests, nine normotensive men (25.9 ± 5.9 years old) and women (24.4 ± 5.9 years old) performed the cold hand pressor test (CPT; 6 min in 5 °C water) in the supine position. A subgroup of men (n = 5) and women (n = 5) from the CPT were exposed to 6 min of facial cooling (FC) by circulating cold water (5 °C) through a perfusion mask. Using standard auscultatory techniques, pre-experimental systolic and diastolic blood pressures were found to be significantly higher (p ≤ 0.05) in males than females. During the initial 2 min of CPT and FC, both males and females experienced similar relative increases in pressure. Thereafter, only the males maintained an elevated pressor response, whereas the females progressively declined. The gender-related trends in blood pressure can be explained by differences in SVR, with the males exhibiting significantly greater changes in SVR than females during min 4–6 in CPT. Heart rate increased (p ≤ 0.05) in both groups, with the greater rise occurring in females at each minute of CPT. Throughout FC, the changes in SVR were similar between groups, with the exception of the 6-min value being greater than baseline in men but not women. No differences in heart rate or cardiac output were observed between groups during FC. In general, the results indicate that men respond with greater and more prolonged peripheral adjustments (e.g., rise in SVR), whereas females are more like "cardiac" responders, with greater increases in heart rate and an attenuated blood pressure response to CPT.Key words: cold pressor test, facial cooling, gender, systemic vascular resistance, heart rate.


2010 ◽  
Vol 108 (6) ◽  
pp. 1591-1594 ◽  
Author(s):  
Scott L. Davis ◽  
Craig G. Crandall

The Valsalva maneuver can be used as a noninvasive index of autonomic control of blood pressure and heart rate. The purpose of this investigation was to test the hypothesis that sympathetic mediated vasoconstriction, as referenced by hemodynamic responses during late phase II (phase IIb) of the Valsalva maneuver, is inhibited during whole body heating. Seven individuals (5 men, 2 women) performed three Valsalva maneuvers (each at a 30-mmHg expiratory pressure for 15 s) during normothermia and again during whole body heating (increase sublingual temperature ∼0.8°C via water-perfused suit). Each Valsalva maneuver was separated by a minimum of 5 min. Beat-to-beat mean arterial blood pressure (MAP) and heart rate were measured during each Valsalva maneuver, and responses for each phase were averaged across the three Valsalva maneuvers for both thermal conditions. Baseline MAP was not significantly different between normothermic (88 ± 11 mmHg) and heat stress (84 ± 9 mmHg) conditions. The change in MAP (ΔMAP) relative to pre-Valsalva MAP during phases IIa and IIb was significantly lower during heat stress (IIa = −20 ± 8 mmHg; IIb = −13 ± 7 mmHg) compared with normothermia (IIa = −1 ± 15 mmHg; IIb = 3 ± 13 mmHg). ΔMAP from pre-Valsalva baseline during phase IV was significantly higher during heat stress (25 ± 10 mmHg) compared with normothermia (8 ± 9 mmHg). Counter to the proposed hypothesis, the increase in MAP from the end of phase IIa to the end of phase IIb during heat stress was not attenuated. Conversely, this increase in MAP tended to be greater during heat stress relative to normothermia ( P = 0.06), suggesting that sympathetic activation may be elevated during this phase of the Valsalva while heat stressed. These data show that heat stress does not attenuate this index of vasoconstrictor responsiveness during the Valsalva maneuver.


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