Chen R Y, Carlin R D, Simchon S, Jan K M, Chien S
Department of Physiology and Cellular Biophysics, College of Physicians and Surgeons, Columbia University, New York, New York 10032.
Am J Physiol. 1989 Mar;256(3 Pt 2):H898-905. doi: 10.1152/ajpheart.1989.256.3.H898.
In 10 pentobarbitalized dogs, plasma viscosity (Ep) was raised fourfold while apparent blood viscosity (Ea) increased about twofold by two steps of exchange transfusion of 200 ml of plasma with plasma containing high molecular weight dextran (mol wt 500,000, 20% wt/vol). Elevation of Ea was primarily caused by an increase of Ep but not red cell aggregation. As Ea increased, regional blood flow (by 15-microns microspheres) remained constant in most organs but reduced in the small intestine, spleen, and thyroid gland. Vascular hindrance (Z), which reflects the state of vascular geometry, was calculated as flow resistance per Ea. Among various organs, a reduction in Z was noted in the heart, liver, pancreas, kidney, brain, and adrenal gland. In myocardium, there was a progressive reduction of the endocardial-to-epicardial flow ratio, indicating a less profound vasodilation in endocardium than epicardium. These results indicate that dextran-induced hyperviscosity leads to a compensatory vasodilation in several vital organs thus serving to maintain blood flow and nutrient transport.
在10只戊巴比妥麻醉的犬中，通过用含有高分子量右旋糖酐（分子量500,000，重量/体积比20%）的血浆分两步置换200ml血浆，血浆粘度（Ep）提高了四倍，而表观血液粘度（Ea）增加了约两倍。Ea升高主要是由Ep增加引起的，而非红细胞聚集所致。随着Ea升高，大多数器官的局部血流（通过15微米微球测量）保持恒定，但小肠、脾脏和甲状腺的血流减少。反映血管几何形态状态的血管阻力（Z）计算为每单位Ea的血流阻力。在各个器官中，心脏、肝脏、胰腺、肾脏、大脑和肾上腺的Z降低。在心肌中，心内膜与心外膜血流比值逐渐降低，表明心内膜的血管舒张程度不如心外膜。这些结果表明，右旋糖酐诱导的高粘度导致几个重要器官出现代偿性血管舒张，从而有助于维持血流和营养物质运输。
