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首页> 外文期刊>American Journal of Physiology >Blood viscosity maintains microvascular conditions during normovolemic anemia independent of blood oxygen-carrying capacity.
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Blood viscosity maintains microvascular conditions during normovolemic anemia independent of blood oxygen-carrying capacity.

机译：血液粘度在正血性贫血期间维持微血管状况，而与血液中的氧气携带能力无关。

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Responses to exchange transfusion with red blood cells (RBCs) containing methemoglobin (MetRBC) were studied in an acute isovolemic hemodiluted hamster window chamber model to determine whether oxygen content participates in the regulation of systemic and microvascular conditions during extreme hemodilution. Two isovolemic hemodilution steps were performed with 6% dextran 70 kDa (Dex70) until systemic hematocrit (Hct) was reduced to 18% (Level 2). A third-step hemodilution reduced the functional Hct to 75% of baseline by using either a plasma expander (Dex70) or blood adjusted to 18% Hct with all MetRBCs. In vivo functional capillary density (FCD), microvascular perfusion, and oxygen distribution in microvascular networks were measured by noninvasive methods. Methylene blue was administered intravenously to reduce methemoglobin (rRBC), which increased oxygen content with no change in Hct or viscosity from MetRBC. Final blood viscosities after the entire protocol were 2.1 cP for Dex70 and 2.8 cP for MetRBC (baseline, 4.2 cP). MetRBC had a greater mean arterial pressure (MAP) than did Dex70. FCD was substantially higher for MetRBC [82 (SD 6) of baseline] versus Dex70 [38 (SD 10) of baseline], and reduction of methemoglobin to oxyhemoglobin did not change FCD [84% (SD 5) of baseline]. P(O2) levels measured with palladium-meso-tetra(4-carboxyphenyl)porphyrin phosphorescence were significantly changed for Dex70 and MetRBC compared with Level 2 (Hct 18%). Reduction of methemoglobin to oxyhemoglobin partially restored P(O2) to Level 2. Wall shear rate and wall shear stress decreased in arterioles and venules for Dex70 and did not change for MetRBC or rRBC. Increased MAP and shear stress-mediated factors could be the possible mechanisms that improved perfusion flow and FCD after exchange for MetRBC. Thus the fall in systemic and microvascular conditions during extreme hemodilution with low-viscosity plasma expanders seems to be, in part, from the decrease in blood viscosity independent of the reduction in oxygen content.
机译：在急性等容血液稀释仓鼠窗室模型中研究了含高铁血红蛋白（MetRBC）的红细胞（RBC）交换输血的反应，以确定在极端血液稀释期间氧含量是否参与系统和微血管状况的调节。用6％的70 kDa右旋糖酐（Dex70）进行两个等容血液稀释步骤，直到全身血细胞比容（Hct）降至18％（2级）。第三步血液稀释通过使用血浆扩展剂（Dex70）或将所有MetRBC的血液调节至18％Hct，将功能性Hct降低至基线的75％。体内功能性毛细血管密度（FCD），微血管灌注和微血管网络中的氧气分布通过无创方法进行了测量。静脉内注射亚甲蓝以减少高铁血红蛋白（rRBC），而高铁血红素增加了氧含量，而Het或MetRBC的粘度没有变化。整个方案后的最终血液粘度对于Dex70为2.1 cP，对于MetRBC为2.8 cP（基线为4.2 cP）。 MetRBC的平均动脉压（MAP）高于Dex70。 MetRBC的FCD显着较高[基线的82（SD 6）]相对于Dex70 [基线的38（SD 10）]，高铁血红蛋白还原为氧合血红蛋白的变化并没有改变FCD [基线的84％（SD 5）]。与水平2（Hct 18％）相比，Dex70和MetRBC的钯-间-四-（4-羧基苯基）卟啉磷光测得的P（O2）水平发生了显着变化。将高铁血红蛋白还原为氧合血红蛋白可将P（O2）部分还原至2级。对于Dex70，小动脉和小静脉的壁切速率和壁切应力降低，而对于MetRBC或rRBC，壁切速率和壁切应力没有变化。 MAP和剪切应力介导的因子增加可能是在换成MetRBC后改善灌注流量和FCD的可能机制。因此，在用低粘度血浆膨胀剂进行极端血液稀释期间，全身和微血管状况的下降似乎部分是由于血液粘度的降低而与氧含量的降低无关。

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