Fónay K, Zámbó K, Radnai B
Sopron Megyei Jogú Város Kórház Mellkasgyógyászati Osztály.
Orv Hetil. 1994 May 8;135(19):1017-21.
Blood viscosity, pressure of pulmonary artery, pulmonary functions, arterial and mixed venous oxygen content, cardiac output, oxygen transport capacity, oxygen consumption, ejection fraction have been examined at 25 patients with or without hypoxic cor pulmonale with or without secondary polycythaemia. Although secondary polycythaemia occurs in patients with hypoxic cor pulmonale as a compensatory process to increase the oxygen carrying capacity of the blood theoretically but as our findings: 1. The rise of haematocrit causes rise in blood viscosity significantly. 2. Polycythaemia secondary over 0.50 l/l of haematocrit contributes the rise of pressure in pulmonary artery. 3. The systemic oxygen carrying capacity is increasing with the rise of haematocrit up to 0.45 l/l but decreasing over 0.50 l/l. 4. Oxygen consumption is decreasing parallel with the rise of haematocrit. 5. Pulmonary functions, cardiac output do not change by the rise of haematocrit.
对25例伴有或不伴有继发性红细胞增多症的低氧性肺心病患者进行了血液粘度、肺动脉压、肺功能、动脉血氧含量和混合静脉血氧含量、心输出量、氧运输能力、氧消耗、射血分数的检查。虽然继发性红细胞增多症在低氧性肺心病患者中作为一种代偿过程出现，理论上可增加血液的携氧能力，但根据我们的研究结果：1. 血细胞比容升高会显著导致血液粘度升高。2. 血细胞比容超过0.50 l/l的继发性红细胞增多症会导致肺动脉压升高。3. 全身氧运输能力随着血细胞比容升高至0.45 l/l而增加，但超过0.50 l/l则下降。4. 氧消耗随着血细胞比容升高而平行下降。5. 血细胞比容升高时肺功能、心输出量不变。
