低氧肺动脉高压大鼠对红细胞增多的适应

目的：研究低氧性肺动脉高压大鼠对实验性红细胞增多的适应。方法：健康SD大鼠28只，体重200～250g，随机分为4组：常氧对照组（N）、单纯低氧组（H）、低氧＋低剂量人重组促红细胞生成素（rEPO）600u／kg（H＋E1）组、低氧＋高剂量rEPO 1200u／kg（H＋E2）组，每组7只大鼠。除常氧对照组外各低氧组大鼠均缺氧21d，每日8h。其中后两组每周腹部皮下注射不同剂量的rEPO三次。取血样测定红细胞数、全血粘度及红细胞变形指数；颈外静脉插管测定平均肺动脉压力；光镜观察反映肺动脉重构程度的形态学参数肺小动脉管壁厚度百分比、肺非肌性小动脉肌化程度。结果：①随着rEPO注射剂量的增加，红细胞、全血粘度有不同程度的增高；②全血粘度增高的同时红细胞变形指数也相应地增加；③随着rEPO剂量的增加，平均肺动脉压力逐渐增高，但是肺血管重构程度反而有所缓解。结论：实验性红细胞增多通过改变红细胞变形性和缓解肺血管重构程度来阻遏低氧性肺动脉高压的进一步发展。

The Adaption of Hypoxia Induced Pulmonary Hypertension to Polycythemia in Rats

Objective：To investigate the adaption of hypoxia induced pulmonary hypertension to polycythemia in rats. Methods.. Twenty-eight healthy female Sprague-Dawley rats （weight 200-250 g） were randomly divided into 4 groups： normoxia control group （group N）, hypoxia group （group H）, hypoxia ＋ low dose human recombination erythropoietin （rEPO） 600 u/kg （group H＋E1）, hypoxia＋ high doser rEPO 1200 u/kg （group H＋E2）. All rats in hyoxia groups were exposed in hypoxia chambers for 8 hours every day for 21 days. The last two groups were injected subcutaneously with different doses of rEPO thrice weekly. On day 21, blood samples were taken for the measurement of RBC, whole blood viscosities and RBC deformation index; the animals were then catheterized to record mean pulmonary arterial pressure （mPAP） ; Morphometric parameters （percentage of vascular wall thickness, muscularization of non-muscular pulmonary arteriole） were examined microscopically to assess the extent of pulmonary artery remodeling. Results： （1）As the dosage of exogenous rEPO increased, RBC, whole blood viscosities increased in various degrees. （2）As the increased of whole blood viscosities, RBC deformation index number increased correspondingly.（3）The degree of pulmonary hypertension, reflected by mPAP increased in accordance to rEPO dosage increment. However, the extent of pulmonary vascular remodeling alleviated somehow as the rEPO dose increased. Conclusion： Experimental polycythemia changes RBC deformation and lessens the degree of pulmonary vascular remodeling, which repressions further development of hypoxia induced pulmonary hypertension.