Liu Chia-Chyuan, Ke Derhin, Chen Zhih-Cherng, Lin Mao-Tsun
Institute of Physiology, National Yang-Ming University, Taipei, Taiwan.
Shock. 2004 Sep;22(3):288-94. doi: 10.1097/01.shk.0000135287.16417.5a.
We hypothesized that hydroxyethyl starch (HES), which maintains colloid osmotic pressure and potentially "seals" capillary leaks, would ameliorate circulatory shock and cerebral ischemia during heatstroke in a rat model. Animals under urethane anesthesia were exposed to high ambient temperature (Ta) of 42 degrees C until mean arterial pressure and local cerebral blood flow in the striatum began to decrease from peak level, which was arbitrarily defined as the onset of heatstroke. Control rats were exposed to 24 degrees C. In rats treated with 1 mL/kg, 11 mL/kg, or 22 mL/kg of normal saline (NS) immediately after the onset of heatstroke, the values for survival time (interval between the initiation of heatstroke and animal death) were found to be 21 +/- 2, 36 +/- 9, or 92 +/- 7 min, respectively. Intravenous administration of 11 mL/kg of HES (about 5 times the volume-expanding effect of 11 mL/kg of NS), but not 2 mL/kg of HES (about the same volume-expanding effect as 11 mL/kg NS), significantly increased the survival time from the control values of 36 +/- 9 min to new values of 181 +/- 13 min. In NS (11 mL/kg)-treated or HES (2 mL/kg)-treated rats after heatstroke onset, the values for mean arterial pressure, stroke volume, total peripheral resistance, cerebral blood flow, blood pH, Paco2, Pao2, and brain Po2 were significantly lower than those of rats kept at Ta 24 degrees C. In contrast, the values for colonic temperature and the extracellular concentrations of glutamate, glycerol, and lactate/pyruvate ratio obtained in striatum were significantly higher than those of controls. The heatstroke-induced arterial hypotension, decreased stroke volume and total peripheral resistance, decreased blood pH and Pao2, decreased brain Po2, and increased levels of striatal glutamate, glycerol, and lactate/pyruvate ratio in NS-treated rats were all attenuated significantly by increasing the volume expansion with 11 mL/kg of HES administered immediately at the onset of heatstroke. Our data suggest that HES therapy seems superior to NS treatment during heatstroke. The benefit of HES therapy during heatstroke might have something to do with volume expansion rather than capillary permeability.
我们推测，羟乙基淀粉（HES）可维持胶体渗透压并可能“封闭”毛细血管渗漏，在大鼠热射病模型中可改善循环性休克和脑缺血。将处于氨基甲酸乙酯麻醉下的动物暴露于42℃的高环境温度（Ta）下，直至平均动脉压和纹状体局部脑血流开始从峰值水平下降，该峰值水平被任意定义为热射病发作。对照大鼠暴露于24℃。在热射病发作后立即用1 mL/kg、11 mL/kg或22 mL/kg生理盐水（NS）处理的大鼠中，存活时间（热射病开始至动物死亡的间隔时间）的值分别为21±2、36±9或92±7分钟。静脉注射11 mL/kg的HES（约为11 mL/kg NS扩容效果的5倍），而不是2 mL/kg的HES（与11 mL/kg NS的扩容效果大致相同），可使存活时间从对照值36±9分钟显著增加至新值181±13分钟。在热射病发作后用NS（11 mL/kg）处理或HES（2 mL/kg）处理的大鼠中，平均动脉压、每搏输出量、总外周阻力、脑血流量、血液pH值、动脉血二氧化碳分压、动脉血氧分压和脑氧分压的值均显著低于饲养在24℃ Ta下的大鼠。相反，在纹状体中测得的结肠温度以及谷氨酸、甘油和乳酸/丙酮酸比值的细胞外浓度值显著高于对照组。热射病诱导的动脉低血压、每搏输出量和总外周阻力降低、血液pH值和动脉血氧分压降低、脑氧分压降低以及NS处理大鼠纹状体中谷氨酸、甘油和乳酸/丙酮酸比值升高，在热射病发作时立即给予11 mL/kg的HES增加扩容后均得到显著缓解。我们的数据表明，在热射病期间，HES治疗似乎优于NS治疗。热射病期间HES治疗的益处可能与扩容有关，而非与毛细血管通透性有关。
