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首页> 外文期刊>American Journal of Physiology >Elevated plasma viscosity in extreme hemodilution increases perivascular nitric oxide concentration and microvascular perfusion.
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Elevated plasma viscosity in extreme hemodilution increases perivascular nitric oxide concentration and microvascular perfusion.

机译：在极端血液稀释中血浆粘度升高会增加血管周围一氧化氮浓度和微血管灌注。

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摘要

We tested the hypothesis that high-viscosity (HV) plasma in extreme hemodilution causes wall shear stress to be greater than low-viscosity (LV) plasma, leading to enhanced production of nitric oxide (NO). The perivascular concentration of NO was measured in arterioles and venules and the tissue of the hamster chamber window model, subjected to acute extreme hemodilution, with a hematocrit (Hct) of 11% using Dextran 500 (n 6) or Dextran 70 (n and 1.33 +/- 0.04 cp, respectively. HV plasma significantly increased the periarteriolar, perivenular, and tissue NO concentration by 2.0, 1.9, and 1.4 times the control (n = 7). The NO concentration with LV plasma was not statistically different from control. Arteriolar shear stress was significantly increased in HV plasma relative to LV plasma in arterioles but not in venules. Aortic endothelial NO synthase (eNOS) protein expression was increased with HV plasma but not with LV plasma. There was a weak correlation between perivascular NO concentration and the locally calculated shear stress induced by the procedures, when blood viscosity was corrected according to Hct values previously determined in studies of microvascular Hct distribution. The finding that the periarteriolar and venular NO concentration in HV plasma was the same although arteriolar shear stress was significantly greater than venular shear stress maybe be due to differences in vessel wall metabolism between arterioles and venules and the presence of NO transport through the blood stream in the microcirculation. Results support the concept that in extreme hemodilution HV plasma maintains functional capillary density through a NO-mediated vasodilatation.
机译：我们测试了以下假设：极端血液稀释中的高粘度（HV）血浆导致壁切应力大于低粘度（LV）血浆，从而导致一氧化氮（NO）产生增加。使用Dextran 500（n 6）或Dextran 70（n和1.33）在小动脉和小静脉以及仓鼠窗玻璃模型的组织中测量NO的血管周围浓度，并进行急性极端血液稀释，血细胞比容（Hct）为11％分别为+/- 0.04 cp。HV血浆显着增加了小动脉周围，周围静脉和组织中NO的浓度，分别为对照组的2.0、1.9和1.4倍（n = 7），LV血浆中的NO浓度与对照组无统计学差异。 HV血浆中的小动脉相对于LV血浆的小动脉切应力显着增加，而小静脉中则没有; LV血浆但不与LV血浆相比，主动脉内皮一氧化氮合酶（eNOS）蛋白表达增加，而血管周NO浓度与LV血浆之间的相关性较弱。当根据先前在微血管Hct分布研究中确定的Hct值校正血液粘度时，由该程序引起的局部计算的切应力。结果发现，尽管血浆小动脉切应力明显大于静脉切应力，但HV血浆中小动脉周围和静脉的NO浓度是相同的，这可能是由于小动脉和小静脉之间的血管壁代谢差异以及NO在血液中通过血流的转运所致。微循环。结果支持这样的概念，即在极端血液稀释中，HV血浆通过NO介导的血管舒张来维持功能性毛细血管密度。

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