Nolte D, Bayer M, Lehr H A, Becker M, Krombach F, Kreimeier U, Messmer K
Institute for Surgical Research, University of Munich, Germany.
Am J Physiol. 1992 Nov;263(5 Pt 2):H1411-6. doi: 10.1152/ajpheart.1992.263.5.H1411.
The underlying mechanisms of the beneficial therapeutic effects of small-volume resuscitation with hyperosmolar solutions for treatment of hypovolemic shock are still poorly understood. Using the dorsal skinfold chamber model and intravital fluorescence microscopy, we investigated the effects of hyperosmolar saline dextran on ischemia-reperfusion injury in striated skin muscle of awake normovolemic golden hamsters. Test solutions (4 ml/kg body wt i.v.) were administered 2 min before reperfusion after 4 h of pressure-induced ischemia. In animals receiving 0.9% saline (control), we observed a drastic enhancement of leukocyte rolling along and sticking to the endothelium of postcapillary venules 0.5 h after reperfusion. Postischemic leukocyte rolling and sticking were significantly reduced when animals were treated with 7.2% saline alone (HSS), 10% Dextran 60 in 0.9% saline (HDS), or 10% Dextran 60 in 7.2% saline (HHS). In control animals, capillary perfusion was reduced to approximately 60% of preischemic values 0.5 h after reperfusion. Concomitantly, leakage of the macromolecule fluorescein isothiocyanate-dextran (5 mg in 0.1 ml saline i.v., M(r) 150,000) into the perivascular space increased from 0% before ischemia to approximately 12% at 0.5 h reperfusion. In contrast, when animals were treated with HSS, HDS, or HHS before reperfusion, capillary perfusion decreased to a significantly minor extent of approximately 15%, and macromolecular leakage was slightly increased to approximately 5%. Our results suggest that hyperosmolar saline dextran effectively attenuates postischemic microvascular disturbances elicited by ischemia-reperfusion, presumably through reduction of postischemic leukocyte-endothelium interaction and capillary swelling.
高渗溶液小容量复苏治疗低血容量性休克的有益治疗效果的潜在机制仍未完全清楚。我们使用背部皮肤褶箱模型和活体荧光显微镜，研究了高渗盐水右旋糖酐对清醒、血容量正常的金黄仓鼠横纹皮肤肌缺血再灌注损伤的影响。在压力诱导缺血4小时后再灌注前2分钟静脉注射测试溶液（4毫升/千克体重）。在接受0.9%盐水（对照）的动物中，我们观察到再灌注后0.5小时白细胞沿毛细血管后微静脉内皮滚动并黏附的现象急剧增强。当动物单独用7.2%盐水（高渗盐水，HSS）、0.9%盐水中的10%右旋糖酐60（高渗右旋糖酐溶液，HDS）或7.2%盐水中的10%右旋糖酐60（高渗高渗右旋糖酐溶液，HHS）治疗时，缺血后白细胞滚动和黏附明显减少。在对照动物中，再灌注后0.5小时毛细血管灌注降至缺血前值的约60%。与此同时，大分子异硫氰酸荧光素 - 右旋糖酐（0.1毫升盐水中5毫克，分子量150,000）向血管周围间隙的渗漏从缺血前的0%增加到再灌注0.5小时时的约12%。相比之下，当动物在再灌注前用HSS、HDS或HHS治疗时，毛细血管灌注仅降至约15%的显著较小程度，大分子渗漏略有增加至约5%。我们的结果表明，高渗盐水右旋糖酐可有效减轻缺血再灌注引起的缺血后微血管紊乱，可能是通过减少缺血后白细胞与内皮的相互作用和毛细血管肿胀来实现的。
