Gustafsson L, Appelgren L, Myrvold H E
Acta Physiol Scand. 1980 Jun;109(2):143-8. doi: 10.1111/j.1748-1716.1980.tb06579.x.
The effect of acutely induced polycythemia on blood flow and viscosity in the vasodilated vascular bed of working and non-working skeletal muscle was studied. In 12 mongrel dogs anesthetized with thiopental sodium the calf muscle of one hind limb was isolated. Vasodilation was induced either by sciatic stimulation setting the muscle at maximal work or by i.a. infusion of papaverine. Blood flow was measured at different perfusion pressure before and after infusion of 300 ml packed homologous red cells. Blood viscosity in vitro was determined in a coneplate viscometer. Apparent viscosity in vivo was analyzed by comparing pressure-flow relationships for blood and a reference solution. Polycythemia decreased blood flow by 35% in the non-working muscle but less than 10% in the working muscle at comparable perfusion pressures. Blood viscosity in vitro increased by 35% at low shear rates. Apparent viscosity in vivo increased by 35% in the non-working muscle but less than 10% in the working muscle. The flow impairment induced by polycythemia was far more pronounced in the non-working skeletal muscle indicating a flow facilitation by the rhythmic muscle contractions. Erythrocyte flow in fact increased in the working muscle after induced polycythemia while decreased in the non-working muscle.
研究了急性诱导的红细胞增多症对工作和不工作的骨骼肌血管舒张床中血流和粘度的影响。在12只硫喷妥钠麻醉的杂种狗中,分离出一侧后肢的小腿肌肉。通过坐骨神经刺激使肌肉处于最大工作状态或通过动脉内注射罂粟碱诱导血管舒张。在输注300ml浓缩同源红细胞前后,在不同灌注压力下测量血流。体外血液粘度在锥板式粘度计中测定。通过比较血液和参考溶液的压力-流量关系分析体内表观粘度。在可比的灌注压力下,红细胞增多症使不工作肌肉的血流减少35%,但使工作肌肉的血流减少不到10%。体外血液粘度在低剪切速率下增加35%。体内表观粘度在不工作肌肉中增加35%,但在工作肌肉中增加不到10%。红细胞增多症引起的血流损害在不工作的骨骼肌中更为明显,表明有节律的肌肉收缩促进了血流。事实上,诱导红细胞增多症后,工作肌肉中的红细胞流动增加,而不工作肌肉中的红细胞流动减少。