Parthasarathi K, Lipowsky H H
Bioengineering Program, The Pennsylvania State University, University Park, Pennsylvania 16802, USA.
Am J Physiol. 1999 Dec;277(6):H2145-57. doi: 10.1152/ajpheart.1999.277.6.H2145.
The effect of reduced red blood cell (RBC) deformability on microvessel recruitment attendant to a reduction in tissue PO2 was studied in rat cremaster muscle using indicator-dilution techniques. Transit times (TT) of fluorescently labeled RBCs (TTRBC) and plasma (TTPl) between functionally paired arterioles and venules were obtained from their dispersion throughout the microvascular network. Changes in PO2 were effected by superfusing the tissue with Ringer solution deoxygenated to different levels. Arteriolar blood flow (Q) was measured with the two-slit technique, and the vascular volume (V) occupied by RBCs and plasma was computed from the product of Q x TT during bolus infusions of rat and less deformable human RBCs to obtain VRBC and fluorescently labeled albumin to obtain VPl. Measurements of TTRBC and TTPl permitted computation of an average flow-weighted tissue (microvascular) hematocrit (HM) relative to systemic values (HS). During infusions of autologous rat RBCs, Q and total V increased threefold in response to hypoxia, whereas normalized RBC TT (TTRBC/TTPl) and normalized tissue hematocrit (HM/HS) did not show a significant trend, indicating an increase in the number of pathways through which the RBCs can traverse the network because of spatial recruitment of capillaries. In contrast, during infusions of human RBCs, TTRBC/TTPl and HM/HS decreased significantly in response to hypoxia. Although Q exhibited an increase similar to that during rat RBC infusions, VRBC exhibited a smaller increase compared with VPl, suggesting that reduced RBC deformability leads to a redistribution of RBCs through larger-diameter pathways within the network and exclusion of these RBCs from pathways normally recruited during hypoxia. Hence, reduced RBC deformability may adversely affect capillary recruitment and physiological mechanisms that ensure adequate delivery of oxygen to tissue.
采用指示剂稀释技术，在大鼠提睾肌中研究了红细胞（RBC）变形性降低对伴随组织氧分压降低的微血管募集的影响。从荧光标记的红细胞（TTRBC）和血浆（TTPl）在功能配对的小动脉和小静脉之间的弥散情况获取其通过微血管网络的转运时间（TT）。通过用不同程度脱氧的林格溶液灌注组织来改变氧分压。用双缝技术测量小动脉血流量（Q），在分别推注大鼠红细胞和变形性较小的人红细胞期间，根据Q×TT的乘积计算红细胞和血浆所占的血管容积（V），以获得VRBC，推注荧光标记白蛋白以获得VPl。测量TTRBC和TTPl可计算相对于全身值（HS）的平均血流加权组织（微血管）血细胞比容（HM）。在输注自体大鼠红细胞期间，缺氧时Q和总V增加了三倍，而标准化的红细胞TT（TTRBC/TTPl）和标准化的组织血细胞比容（HM/HS）没有显示出显著变化趋势，这表明由于毛细血管的空间募集，红细胞穿越网络的途径数量增加。相反，在输注人红细胞期间，缺氧时TTRBC/TTPl和HM/HS显著降低。尽管Q的增加与输注大鼠红细胞期间相似，但与VPl相比，VRBC的增加较小，这表明红细胞变形性降低导致红细胞通过网络中较大直径的途径重新分布，并将这些红细胞排除在缺氧时通常募集的途径之外。因此，红细胞变形性降低可能会对毛细血管募集和确保向组织充分输送氧气的生理机制产生不利影响。
