Nolte D, Botzlar A, Pickelmann S, Bouskela E, Messmer K
Institute for Surgical Research, Klinikum Grosshadern, Ludwig-Maximilians-University of Munich, Germany.
J Lab Clin Med. 1997 Sep;130(3):314-27. doi: 10.1016/s0022-2143(97)90027-5.
Hemoglobin-based oxygen-carrying solutions are reported to exert vasoconstrictor effects and to enhance oxygen radical formation, particularly during ischemia-reperfusion. This study investigates whether diaspirin-cross-linked hemoglobin (DCLHb) affects the microvascular integrity of striated skin muscle. The microcirculation model in the hamster and intravital fluorescence microscopy were applied for investigation of the microvascular changes in striated skin muscle. Hypervolemic infusion (500 mg x kg(-1), I.V.) and isovolemic exchange transfusion (3.3 gm x kg(-1) I.V.; hematocrit 30%) with DCLHb (1) led to a short-lasting (0 to 2 minutes) arteriolar constriction (approximately 20% reduction in baseline diameter), (2) significantly influenced arteriolar vasomotion, (3) increased venular red blood cell velocity by 1.5-fold (p < 0.05 vs dextran, Mr 60,000), and (4) did not enhance microvascular leukocyte-endothelium interaction or endothelial permeability. Resuscitation from severe hemorrhagic shock with autologous blood (AuB) or DCLHb (33 ml x kg(-1), I.V.) immediately restored mean arterial pressure and heart rate, whereas 6% dextran (60 kd)(Dx-60) did not return these parameters to baseline. Venular red blood cell velocity was restored to 110% of baseline after DCLHb, to 90% of baseline after AuB, and to 45% of baseline after Dx-60. Leukocyte-endothelium interaction was significantly enhanced after resuscitation with AuB and Dx-60, whereas this phenomenon was absent after DCLHb. These data demonstrate that DCLHb increases venular red blood cell velocity under both nonischemic and postischemic conditions without inducing enhanced leukocyte-endothelium interaction in the microcirculation of striated skin muscle.
据报道，基于血红蛋白的携氧溶液具有血管收缩作用，并能增强氧自由基的形成，尤其是在缺血再灌注期间。本研究调查了双阿司匹林交联血红蛋白（DCLHb）是否会影响横纹皮肤肌肉的微血管完整性。采用仓鼠微循环模型和活体荧光显微镜技术来研究横纹皮肤肌肉的微血管变化。用DCLHb进行高血容量输注（500 mg·kg⁻¹，静脉注射）和等血容量交换输血（3.3 g·kg⁻¹静脉注射；血细胞比容30%）（1）导致小动脉短暂收缩（0至2分钟）（基线直径降低约20%），（2）显著影响小动脉血管运动，（3）使小静脉红细胞速度提高1.5倍（与60000分子量的右旋糖酐相比，p < 0.05），以及（4）未增强微血管白细胞与内皮细胞的相互作用或内皮通透性。用自体血（AuB）或DCLHb（33 ml·kg⁻¹，静脉注射）对严重失血性休克进行复苏后，平均动脉压和心率立即恢复，而6%的右旋糖酐（60 kd）（Dx - 60）未能使这些参数恢复到基线水平。DCLHb治疗后小静脉红细胞速度恢复到基线的110%，AuB治疗后恢复到基线的90%，Dx - 60治疗后恢复到基线的45%。用AuB和Dx - 60复苏后，白细胞与内皮细胞的相互作用显著增强，而DCLHb治疗后未出现这种现象。这些数据表明，DCLHb在非缺血和缺血后条件下均可增加小静脉红细胞速度，且不会在横纹皮肤肌肉微循环中诱导增强的白细胞与内皮细胞相互作用。
