Langenfeld J E, Machiedo G W, Lyons M, Rush B F, Dikdan G, Lysz T W
Department of Surgery, UMD-New Jersey Medical School, Newark 07103.
Surgery. 1994 Nov;116(5):859-67.
In sepsis red blood cells (RBCs) have been shown to be less deformable (i.e., more rigid) and have been implicated in decreasing nutrient blood supply and possibly leading to organ dysfunction. However, no studies have demonstrated an association between organ dysfunction and rigid RBCs. This study examined cardiovascular physiologic and histologic changes in two different models to determine whether a relationship may exist between RBC deformability and organ function.
In the following two experiments, cardiac index (CI) was continuously measured, whereas both deformability index and histology were examined at the end of the experimental periods. The first experiment studied nonanesthetized, hydrated rats after a cecal ligation and puncture (CLP), a slow-developing means of inducing RBC rigidity. In a second experiment animals were anesthetized and received a 20% total blood volume transfusion of either diamide-treated (rigid) RBCs or normal RBCs.
CLP-treated animals' CI gradually decreased during 18 hours (232 +/- 60 ml/min/kg to 123 +/- 90 ml/min/kg; p = 0.05), with an increase in systemic vascular resistance (1459 +/- 517 dyne.sec/cm5.m2 to 2337 +/- 1213 dyne.sec/cm5.m2; p = 0.02). Diamide-treated animals had a rapid decrease in CI (86 +/- 7.0 ml/min/kg to 58 +/- 13 ml/min/kg; p = 0.05) and increase in SVR (2269 +/- 373 dyne.sec/cm5.m2 to 3897 +/- 988 dyne.sec/cm5.m2; p = 0.05) from baseline to 120 minutes after treatment respectively. The DI was significantly lower in both CLP and diamide groups (p < 0.03) when compared with control animals. Histologic evidence of subendocardial necrosis was shown in both the CLP- and Diamide-treated animals.
These data suggest an association with RBC deformability and organ function in both septic and nonseptic animal models.
在脓毒症中，红细胞（RBCs）已被证明变形能力降低（即更僵硬），这与营养物质血液供应减少有关，并可能导致器官功能障碍。然而，尚无研究证明器官功能障碍与僵硬的红细胞之间存在关联。本研究在两种不同模型中检测心血管生理和组织学变化，以确定红细胞变形能力与器官功能之间是否可能存在关系。
在以下两个实验中，持续测量心脏指数（CI），而在实验期结束时检测变形能力指数和组织学。第一个实验研究了经盲肠结扎和穿刺（CLP）的未麻醉、补水大鼠，这是一种诱导红细胞僵硬的缓慢发展方式。在第二个实验中，动物被麻醉，并接受20%全血容量的二酰胺处理（僵硬）红细胞或正常红细胞输血。
CLP处理的动物在18小时内CI逐渐降低（从232±60 ml/min/kg降至123±90 ml/min/kg；p = 0.05），全身血管阻力增加（从1459±517达因·秒/厘米⁵·平方米增至2337±1213达因·秒/厘米⁵·平方米；p = 0.02）。二酰胺处理的动物从基线到处理后120分钟CI迅速降低（从86±7.0 ml/min/kg降至58±13 ml/min/kg；p = 0.05），SVR增加（从2269±373达因·秒/厘米⁵·平方米增至3897±988达因·秒/厘米⁵·平方米；p = 0.05）。与对照动物相比，CLP组和二酰胺组的变形能力指数均显著降低（p < 0.03）。CLP处理和二酰胺处理的动物均出现心内膜下坏死的组织学证据。
这些数据表明，在脓毒症和非脓毒症动物模型中，红细胞变形能力与器官功能之间存在关联。
