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Heat stress attenuates increases in arterial blood pressure during a cold pressor test (CPT)
Author(s) -
Cui Jian,
Shibasaki Manabu,
Low David,
Keller David,
Davis Scott,
Crandall Craig
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a563-c
Subject(s) - blood pressure , heart rate , orthostatic intolerance , cold pressor test , orthostatic vital signs , medicine , anesthesia , mean arterial pressure , hemodynamics , heat stress , thermoregulation , cold stress , chemistry , zoology , biology , biochemistry , gene
Heat stress impairs orthostatic tolerance and “sympatholysis” may contribute to this response. This study tested the hypothesis that whole body heating (WBH) attenuates the increase in mean arterial blood pressure (MAP) to CPT‐induced sympathetic activation. Muscle sympathetic nerve activity (MSNA), MAP, and ECG were recorded in 9 healthy subjects. A CPT was performed by immersing a hand in ice water for 3 min during both normothermic and WBH conditions. WBH significantly increased core temperature ~0.7 °C, heart rate (60 ± 3 to 85 ± 3 bpm, p<0.001) and MSNA (13.4 ± 2.1 to 23.2 ± 3.4 bursts/min, p=0.005), but did not significantly alter MAP (p=0.245). In both thermal conditions, CPT induced significant increases in MSNA and MAP without altering heart rate. In normothermia, the increase in MAP by the CPT was larger relative to during WBH (Δ28 ± 3 vs Δ18 ± 3 mmHg, p=0.005). However, similar increases in MSNA between thermal conditions (normothermia: Δ15 ± 3, WBH: Δ20 ± 2 bursts/min, p=0.145) suggests similar levels of sympathoexcitation by the CPT. Attenuated increases in blood pressure to similar CPT‐induced increases in vasoconstrictor neural activity suggests that heat stress has the capacity to alter neural control of blood pressure. This impairment may contribute to orthostatic intolerance in heat stressed individuals. Supported by NIH HL61388, HL67422, & HL84072 and AHA 0635245N.