Geometric resistance to blood flow in solid tumors perfused ex vivo: effects of tumor size and perfusion pressure.
Geometric resistance to blood flow in solid tumors perfused ex vivo: effects of tumor size and perfusion pressure.
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发表时间：
1989-07
期刊：
影响因子：
11.2
通讯作者：
E. Sevick;Rakesh K. Jain
中科院分区：
文献类型：
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作者：
E. Sevick;Rakesh K. Jain
在血管网络中，血液流速与动静脉压差成正比，与粘性阻力和几何阻力成反比。通过灌注组织分离的乳腺癌，测定肿瘤血流的几何阻力（R3230 AC; N = 40;肿瘤重量，1.8 +/- 1.2（SD）g;范围，0.5- 6.6g）离体用无细胞Krebs-Henseleit培养基（粘度，0.9 g/m/s），速率为0.1至60 ml/h，动静脉压差为0至120 mm Hg。低于40 mm Hg的灌注压，压力-流量行为总是非线性的，表明几何阻力升高，血管横截面积随着微血管压力的降低而减少。然而，在40 mm Hg以上，压力-流量行为是线性的，证明了恒定的几何阻力z 0和恒定的流动血管横截面积。当肿瘤重量从0.5增加到6.6 g时，z 0从1.6增加到17.3 × 10（8）g/cm 3。z 0对肿瘤大小的这种依赖性与体内观察到的肿瘤灌注率随肿瘤生长而降低一致。与之前对正常器官和组织的研究相比，肿瘤中的z 0可以高出1-2个数量级，具体取决于肿瘤重量。这种几何阻力对灌注压和肿瘤大小的依赖性为肿瘤微循环动力学提供了新的见解，并具有重要的临床意义。
In a vascular network blood flow rate is proportional to the arteriovenous pressure difference and inversely proportional to the viscous and geometric resistances. The geometric resistance to tumor blood flow was determined by perfusing tissue-isolated mammary adenocarcinoma (R3230AC; N = 40; tumor weight, 1.8 +/- 1.2 (SD) g; range, 0.5-6.6 g) ex vivo with an acellular Krebs-Henseleit medium (viscosity, 0.9 g/m/s) at rates of 0.1 to 60 ml/h and arteriovenous pressure differences of 0 to 120 mm Hg. Below perfusion pressures of 40 mm Hg, pressure-flow behavior was always nonlinear, indicating elevated geometric resistance and a reduction in vascular cross-sectional area with decreasing microvessel pressure. However, above 40 mm Hg, pressure-flow behavior was linear demonstrating a constant geometric resistance, z0 and a constant vascular cross-sectional area for flow. z0 increased linearly from 1.6 to 17.3 X 10(8) g/cm3 as tumor weight increased from 0.5 to 6.6 g. This dependence of z0 upon tumor size is in agreement with the decrease in tumor perfusion rates with tumor growth observed in vivo. Comparison with previous studies of normal organs and tissues shows that z0 in tumors can be as much as 1-2 orders of magnitude higher, depending upon tumor weight. This dependence of geometric resistance on perfusion pressure and tumor size offers novel insights into the dynamics of tumor microcirculation and has significant clinical implications.