Bauer M, Marzi I, Ziegenfuss T, Seeck G, Bühren V, Larsen R
Clinic for Anesthesiology and Critical Care Medicine, University of Saarland, Homburg, Germany.
Circ Shock. 1993 Jul;40(3):187-93.
Hepatic microcirculation, leukocyte-endothelial interaction, and sinusoidal widths were studied by means of intravital microscopy in a non-heparinized fixed pressure hemorrhagic shock model in the rat. Asanguineous resuscitation was performed either with "adequate" amounts of lactated Ringer's solution (threefold shed volume/30 min) or 4 ml/kg/3 min 7.2% saline/10% Dextran 60 (HSDex) or 4 ml/kg/3 min 7.2% saline/10% hydroxyethylstarch 200/0.62 (HSHes). Hemorrhagic shock and resuscitation was paralleled by significant (P < 0.01) lumenal narrowing of sinusoids that remained largely uninfluenced by the type of fluid used for resuscitation (HSDex: 9.28 +/- 0.56; HSHes: 8.93 +/- 0.29, LR: 8.87 +/- 0.6 microns compared to 12.17 +/- 0.24 microns in controls). Whereas HSHes and LR-therapy resulted in comparably increased leukocyte adhesion to the sinusoidal wall, the dextran-containing solution led to a significant attenuation of leukocyte-endothelial interaction, suggesting involvement of dextran-binding adhesion molecules, e.g., selectins.
在大鼠非肝素化固定压力失血性休克模型中,通过活体显微镜研究肝微循环、白细胞与内皮细胞的相互作用以及肝血窦宽度。分别用“足量”乳酸林格液(失血量的三倍/30分钟)、4毫升/千克/3分钟的7.2%盐水/10%右旋糖酐60(HSDex)或4毫升/千克/3分钟的7.2%盐水/10%羟乙基淀粉200/0.62(HSHes)进行无血复苏。失血性休克和复苏过程中,肝血窦管腔显著狭窄(P < 0.01),且这种狭窄在很大程度上不受复苏所用液体类型的影响(HSDex组:9.28±0.56;HSHes组:8.93±0.29;乳酸林格液组:8.87±0.6微米,而对照组为12.17±0.24微米)。尽管HSHes和乳酸林格液治疗导致白细胞与肝血窦壁的黏附同样增加,但含右旋糖酐的溶液使白细胞与内皮细胞的相互作用显著减弱,提示右旋糖酐结合黏附分子(如选择素)参与其中。