Chien S
Department of Physiology and Cellular Biophysics, Columbia University College of Physicians and Surgeons, New York, NY 10032.
Biorheology. 1986;23(6):633-53. doi: 10.3233/bir-1986-23614.
Blood rheology was studied in patients with acute myocardial infarction (AMI) and essential hypertension (EH), and the results were correlated with in vivo hemodynamic functions. Blood viscosity (eta B) was elevated as a result of sequential changes of a number of parameters, including increases in hematocrit, plasma fibrinogen and alpha 2-globulin, an enhancement of red cell aggregation and a reduction of red cell filterability in plasma. Total peripheral resistance (TPR) was elevated upon admission, due to increases in both the vascular hindrance (ZS) and eta B. During recovery, the eta B became normalized; alterations in eta B were accompanied by parallel changes in TPR and an inverse change in plasma volume (PV). In EH patients, the increase in eta B showed a correlation with arterial pressure. For both established and borderline hypertensives, the rheological changes were most prominent in the high renin subgroups. In mild EH, the elevation of eta B was compensated by a decrease in ZS (vasodilation), keeping the TPR essentially normal. In EH with higher arterial pressure, the elevation of eta B was accompanied by a normal ZS without compensatory vasodilation, and hence TPR rose to exacerbate the hypertension. These results suggest that the elevation of eta B may be an early event in the development of EH and that its role must be considered with concurrent cardiovascular functions. In EH there is a significant correlation between left ventricular mass and eta B. Experimental manipulations of the hematocrit level in spontaneously hypertensive rats led to a corresponding variation of arterial pressure. The available data implicate a significant role of eta B in the pathophysiology of AMI and EH. Further interdisciplinary, longitudinal studies are needed tin order to unravel the complicated pathophysiological changes in myocardial infarction and hypertension.
对急性心肌梗死（AMI）和原发性高血压（EH）患者的血液流变学进行了研究，并将结果与体内血流动力学功能相关联。由于包括血细胞比容、血浆纤维蛋白原和α2球蛋白增加、红细胞聚集增强以及血浆中红细胞滤过率降低等多个参数的相继变化，血液粘度（ηB）升高。入院时，由于血管阻力（ZS）和ηB均增加，总外周阻力（TPR）升高。在恢复过程中，ηB恢复正常；ηB的变化伴随着TPR的平行变化和血浆容量（PV）的反向变化。在EH患者中，ηB的升高与动脉压相关。对于确诊高血压患者和临界高血压患者，血液流变学变化在高肾素亚组中最为显著。在轻度EH中，ηB的升高通过ZS降低（血管舒张）得到补偿，使TPR基本保持正常。在动脉压较高的EH患者中，ηB的升高伴随着ZS正常但无代偿性血管舒张，因此TPR升高加剧了高血压。这些结果表明，ηB的升高可能是EH发生发展中的早期事件，其作用必须与同时存在的心血管功能一并考虑。在EH患者中，左心室质量与ηB之间存在显著相关性。对自发性高血压大鼠血细胞比容水平进行实验性操作导致动脉压相应变化。现有数据表明ηB在AMI和EH的病理生理学中起重要作用。需要进一步开展跨学科的纵向研究，以阐明心肌梗死和高血压中复杂的病理生理变化。
