血管活性药物丁咯地尔减少缺血后再灌注损伤。

Blood vessels Pub Date : 1991-01-01 DOI:10.1159/000158913
D Nolte, H A Lehr, F U Sack, K Messmer
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引用次数: 12

摘要

研究了丁咯地尔对清醒仓鼠背侧皮肤褶腔制备后缺血再灌注损伤的影响。用活体荧光显微镜观察压力致缺血4小时和再灌注30分钟、2小时和24小时后横纹肌的微血管事件。在未处理的对照动物中,缺血和再灌注引起明显的白细胞粘附和大分子泄漏,而功能毛细血管密度降低。buflomedil (3 mg/kg b.w.加入0.3 ml生理盐水中,在缺血释放前10分钟给药0.1 ml,再灌注后20分钟静脉滴注0.2 ml)可显著减少白细胞粘附和大分子渗漏,同时有效保持功能性毛细血管密度。在布洛地地治疗和未治疗的动物之间,宏观和微观血流动力学参数没有观察到差异。这些发现支持了活化的白细胞参与再灌注损伤微血管表现的观点,并提示buflomedil治疗可有效预防白细胞粘附及其后遗症。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Reduction of postischemic reperfusion injury by the vasoactive drug buflomedil.

The effect of buflomedil on postischemic reperfusion injury was studied in the dorsal skin fold chamber preparation of awake hamsters. Microvascular events were investigated in the striated skin muscle by means of intravital fluorescence microscopy prior to 4 h of pressure-induced ischemia and 30 min, 2 and 24 h after reperfusion. In untreated control animals, ischemia and reperfusion provoked marked leukocyte sticking and macromolecular leakage while functional capillary density was reduced. Treatment with buflomedil (3 mg/kg b.w. in 0.3 ml saline, administered as bolus of 0.1 ml 10 min prior to release of ischemia followed by i.v. infusion of 0.2 ml during the first 20 min of reperfusion) significantly reduced leukocyte sticking and macromolecular leakage, while functional capillary density was effectively preserved. No differences in macro- and microhemodynamic parameters were observed between buflomedil-treated and untreated animals. These findings support the concept that activated leukocytes are involved in the microvascular manifestation of reperfusion injury and indicate that leukocyte sticking and its sequelae can be efficiently prevented by treatment with buflomedil.

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