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The systemic vascular resistance response: a cardiovascular response modulating blood viscosity with implications for primary hypertension and certain anemias

机译:全身性血管阻力反应:调节血液粘度的心血管反应,与原发性高血压和某些贫血有关

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Without an active regulatory feedback loop, increased blood viscosity could lead to a vicious cycle of ischemia, increased erythropoiesis, further increases of blood viscosity, decreased tissue perfusion with worsened ischemia, further increases in red cell mass, etc. We suggest that an increase in blood viscosity is detected by mechanoreceptors in the left ventricle which upregulate expression of cardiac natriuretic peptides and soluble erythropoietin receptor. This response normalizes systemic vascular resistance and blood viscosity at the cost of producing ‘anemia of chronic disease or inflammation’ or ‘hemolytic anemia’ both of which are better described as states of compensated hyperviscosity. Besides its role in disease, this response is also active in the physiologic adaptation to chronic exercise. Malfunction of this response may cause primary hypertension.
机译:没有有效的调节反馈回路,血液粘度增加可能导致缺血的恶性循环,红细胞生成增加,血液粘度进一步增加,组织灌注减少,局部缺血恶化,红细胞量进一步增加等。我们建议增加通过左心室中的机械感受器检测血液粘度,所述机械感受器上调心脏利钠肽和可溶性促红细胞生成素受体的表达。这种反应以产生“慢性病或炎症性贫血”或“溶血性贫血”为代价,使全身血管阻力和血液粘度正常化,这两种状态都可以更好地描述为代偿性高粘度状态。除了其在疾病中的作用外,该反应还对慢性运动的生理适应性起作用。该反应的功能障碍可能会导致原发性高血压。

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