Crandall C G, Wilson T E, Marving J, Vogelsang T W, Kjaer A, Hesse B, Secher N H
Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas, 7232 Greenville Avenue, Dallas, TX 75231, USA.
J Physiol. 2008 Jan 1;586(1):293-301. doi: 10.1113/jphysiol.2007.143057. Epub 2007 Oct 25.
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 seven 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 labelled autologous red blood cells and gamma camera imaging. Whole-body heating increased internal temperature (> 1.0 degrees C), cutaneous vascular conductance (approximately fivefold), and heart rate (52 +/- 2 to 93 +/- 4 beats min(-1)), while reducing central venous pressure (5.5 +/- 07 to 0.2 +/- 0.6 mmHg) accompanied by minor decreases in mean arterial pressure (all P < 0.05). The heat stress reduced the 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 from 60 +/- 1% to 68 +/- 2% (P = 0.02). We conclude 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.
关于全身热应激对中心血容量的影响,已有混合性的研究结果报道。本研究评估了热应激会降低中心血容量并改变血容量分布这一假设。十名健康的实验对象和七名健康的时间对照组(即非热应激)对象参与了本实验方案。在热应激和时间对照期间,使用锝-99m标记的自体红细胞和γ相机成像来估计局部血容量的变化。全身加热使体内温度升高(>1.0摄氏度)、皮肤血管传导性增加(约五倍)以及心率加快(从52±2次/分钟增加至93±4次/分钟),同时中心静脉压降低(从5.5±0.7毫米汞柱降至0.2±0.6毫米汞柱),平均动脉压也有轻微下降(所有P<0.05)。热应激使心脏的血容量减少(18±2%)、心脏加中心血管系统的血容量减少(17±2%)、胸部的血容量减少(14±2%)、下腔静脉的血容量减少(23±2%)以及肝脏的血容量减少(23±2%)(相对于时间对照组对象,所有P≤0.005)。放射性核素多门控采集评估显示,热应激并未显著改变左心室舒张末期容积,而心室收缩末期容积比热应激前水平降低了24±6%(相对于时间对照组对象,P<0.001)。因此,热应激使左心室射血分数从60±1%增加至68±2%(P=0.02)。我们得出结论,热应激使血容量从胸部和内脏区域转移,大概是为了帮助散热,同时增加心率和射血分数。