Tsai A G, Friesenecker B, McCarthy M, Sakai H, Intaglietta M
Department of Bioengineering, University of California, San Diego, La Jolla, California 92093-0412, USA.
Am J Physiol. 1998 Dec;275(6):H2170-80. doi: 10.1152/ajpheart.1998.275.6.H2170.
Effect of increasing blood viscosity during extreme hemodilution on capillary perfusion and tissue oxygenation was investigated in the awake hamster skinfold model. Two isovolemic hemodilution steps were performed with 6% Dextran 70 [molecular weight (MW) = 70,000] until systemic hematocrit (Hct) was reduced by 65%. A third step reduced Hct by 75% and was performed with the same solution [low viscosity (LV)] or a high-molecular-weight 6% Dextran 500 solution [MW = 500, 000, high viscosity (HV)]. Final plasma viscosities were 1.4 and 2.2 cP (baseline of 1.2 cP). Hct was reduced to 11.2 +/- 1.1% from 46.2 +/- 1.5% for LV and to 11.9 +/- 0.7% from 47.3 +/- 2.1% for HV. HV produced a greater mean arterial blood pressure than LV. Functional capillary density (FCD) was substantially higher after HV (85 +/- 12%) vs. LV (38 +/- 30%) vs. baseline (100%). PO2 levels measured with Pd-porphyrin phosphorescence microscopy were not statistically changed from baseline until after the third hemodilution step. Wall shear rate (WSR) decreased in arterioles and venules after LV and only in arterioles after HV. Wall shear stress (WSR x plasma viscosity) was substantially higher after HV vs. LV. Increased mean arterial pressure and shear stress-dependent release of endothelium-derived relaxing factor are possible mechanisms that improved arteriolar and venular blood flow and FCD after HV vs. LV exchange protocols.
在清醒的仓鼠皮肤褶模型中,研究了在极重度血液稀释过程中血液粘度增加对毛细血管灌注和组织氧合的影响。使用6%右旋糖酐70(分子量(MW)=70,000)进行了两个等容血液稀释步骤,直到全身血细胞比容(Hct)降低65%。第三步将Hct降低75%,使用相同溶液[低粘度(LV)]或高分子量6%右旋糖酐500溶液[MW = 500,000,高粘度(HV)]进行。最终血浆粘度分别为1.4和2.2厘泊(基线为1.2厘泊)。LV组Hct从46.2±1.5%降至11.2±1.1%,HV组从47.3±2.1%降至11.9±0.7%。HV组产生的平均动脉血压高于LV组。与LV组(38±30%)和基线(100%)相比,HV组后的功能性毛细血管密度(FCD)显著更高(85±12%)。用钯卟啉磷光显微镜测量的PO2水平在第三次血液稀释步骤之前与基线相比无统计学变化。LV组后小动脉和小静脉的壁剪切率(WSR)降低,HV组仅小动脉的WSR降低。HV组后的壁剪切应力(WSR×血浆粘度)显著高于LV组。平均动脉压升高和内皮衍生舒张因子的剪切应力依赖性释放可能是在HV与LV交换方案后改善小动脉和小静脉血流及FCD的机制。