School of Medicine, Royal College of Surgeons, Dublin, Ireland.
Biomech Model Mechanobiol. 2011 Jul;10(4):591-8. doi: 10.1007/s10237-010-0258-y. Epub 2010 Sep 29.
The level of hematocrit (Hct) is known to affect mean arterial pressure (MAP) by influencing blood viscosity. In the healthy population, an increase in Hct (and corresponding increase in viscosity) tends to raise MAP. However, data from a clinical study of type 2 diabetic patients indicate that this relationship is not universal. Instead, individuals in the lower levels of Hct range display a decrease in MAP for a given rise in Hct. After reaching a minimum, this trend is reversed, so that further increases in Hct lead to increases in MAP. We hypothesize that this anomalous behavior occurs due to changes in the circulatory autoregulation mechanism. To substantiate this hypothesis, we develop a physically based mathematical model that incorporates autoregulation mechanisms. Our model replicates the anomalous U-shaped relationship between MAP and Hct found in diabetic patients in the same range of Hct variability.
血细胞比容(Hct)的水平已知会通过影响血液粘度来影响平均动脉压(MAP)。在健康人群中,Hct 的增加(以及相应的粘度增加)往往会导致 MAP 升高。然而,来自 2 型糖尿病患者临床研究的数据表明,这种关系并非普遍存在。相反,在给定的 Hct 升高范围内,Hct 水平较低的个体的 MAP 会下降。达到最低点后,这种趋势发生逆转,因此 Hct 的进一步增加会导致 MAP 的增加。我们假设这种异常行为是由于循环自动调节机制的变化引起的。为了证实这一假设,我们开发了一个基于物理的数学模型,其中包含自动调节机制。我们的模型复制了在相同 Hct 变化范围内糖尿病患者中发现的 MAP 和 Hct 之间异常的 U 形关系。