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Received August 15, 2007
Revised September 12, 2007
Accepted after revision October 23, 2007
1 Presbyterian Hospital of Dallas; University of Texas Southwestern Medical Center
2 Drexel University College of Medicine
3 Rigshospitalet University Hospital, University of Copenhagen
* To whom correspondence should be addressed. E-mail: craigcrandall{at}texashealth.org.
Mixed findings regarding the effects of whole-body heat stress on central blood volume have been reported. This study evaluated the hypothesis that heat stress reduces central blood volume and alters blood volume distribution. Ten healthy experimental and 7 healthy time control (i.e. non-heat stressed) subjects participated in this protocol. Changes in regional blood volume during heat stress and time control were estimated using technetium-99m labeled autologous red blood cells and gamma camera imaging. Whole-body heating increased internal temperature >1.0 °C, cutaneous vascular conductance approximately five fold, and heart rate (52±2 to 93±4 bpm), while reducing central venous pressure (5.5±07 to 0.2±0.6 mmHg) accompanied with minor decreases in mean arterial pressure (all P<0.05). This heat stress reduced blood volume of the heart (18±2%), heart plus central vasculature (17±2%), thorax (14±2%), inferior vena cava (23±2%), and liver (23±2%) (all P
0.005 relative to time control subjects). Radionuclide multiple gated acquisition assessment revealed that heat stress did not significantly change left ventricular end-diastolic volume, while ventricular end-systolic volume was reduced by 24±6% of pre-heat stress levels (P<0.001 relative to time control subjects). Thus, heat stress increased left ventricular ejection fraction LVEF from 60±1% to 68±2% (P=0.02). These data demonstrate that heat stress shifts blood volume from thoracic and splanchnic regions presumably to aid in heat dissipation, while simultaneously increasing heart rate and ejection fraction.
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