Nihill M R, McNamara D G, Vick R L
Am Heart J. 1976 Jul;92(1):65-72. doi: 10.1016/s0002-8703(76)80404-8.
The isolated left lower lobes of 15 dogs' lungs were perfused by means of a roller pump with blood at hematocrit values ranging from 31 to 80 per cent. Pressure-flow curves were constructed at blood flow rates from one half to three times the normal flow for the left lower lobe at each hematocrit level. The perfusion pressure was normalized with reference to the normal hematocrit(38 to 48 per cent) and normal blood flow for the left lower lobe (20 ml. per kilogram per minute). From these normalized pressure-flow curves, normalized resistance-flow curves were constructed at different mean hematocrit levels. Regression lines were drawn relating normalized pulmonary vascular resistance to hematocrit at different rates of pulmonary blood flow which might be found in patients with congenital heart disease. It was found that pulmonary vascular resistance rose in an exponential fashion as the hematocrit was increased, and that the blood viscosity determined both the shape of the resistance-flow curve and magnitude of the increase in resistance to pulmonary blood flow, especially when the pulmonary blood flow was less than normal and the hematocrit was greater than 54 per cent. The family of regression lines relating pulmonary vascular resistance to hematocrit at different flow rates may be used clinically in patients with congenital heart disease and polycythemia to determine if an elevated pulmonary vascular resistance is due to increased blood viscosity or obstructive pulmonary vascular disease. It is concluded that an increased blood viscosity due to polycythemia significantly alters the pulmonary hemodynamics of patients with congenital heart disease with either increased or decreased pulmonary blood flow. Increased blood viscosity may play an important part in the early initiation and development of pulmonary arteriosclerosis in patients with transposition of the great arteries.
用滚轴泵以血细胞比容值在31%至80%范围内的血液灌注15只狗的离体左下肺叶。在每个血细胞比容水平下,以左下肺叶正常血流量的一半至三倍的血流速率绘制压力 - 流量曲线。灌注压力参照正常血细胞比容(38%至48%)和左下肺叶正常血流量(每千克每分钟20毫升)进行标准化。根据这些标准化的压力 - 流量曲线,在不同的平均血细胞比容水平下绘制标准化阻力 - 流量曲线。绘制了不同肺血流速率下,先天性心脏病患者可能出现的标准化肺血管阻力与血细胞比容之间的回归线。结果发现,随着血细胞比容的增加,肺血管阻力呈指数上升,并且血液粘度既决定了阻力 - 流量曲线的形状,也决定了肺血流阻力增加的幅度,特别是当肺血流量低于正常且血细胞比容大于54%时。不同血流速率下肺血管阻力与血细胞比容之间的回归线族可在临床上用于先天性心脏病和红细胞增多症患者,以确定肺血管阻力升高是由于血液粘度增加还是阻塞性肺血管疾病所致。得出的结论是,红细胞增多症导致的血液粘度增加会显著改变先天性心脏病患者肺血流量增加或减少时的肺血流动力学。血液粘度增加可能在大动脉转位患者肺动脉硬化的早期发生和发展中起重要作用。