Peter F W, Schuschke D A, Wang W Z, Anderson G L, Franken R J, Pierangeli S, Barker J H
Division of Plastic and Reconstructive Surgery, University of Louisville School of Medicine, KY, USA.
Microsurgery. 1998;18(1):23-8. doi: 10.1002/(sici)1098-2752(1998)18:1<23::aid-micr6>3.0.co;2-v.
Impaired capillary perfusion may result in flap failure. Platelet emboli, polymorphonuclear leukocytes (PMNs), and/or vasospasm have been identified as possible causes. This study investigates the role of PMNs in causing impaired capillary perfusion in a free flap model. PMN concentrations were depleted using antineutrophil serum. The cremaster muscles of 20 Sprague-Dawley rats were isolated on a single neurovascular pedicle and after a simulated technically poor arterial anastomosis upstream and reperfusion, capillary perfusion was measured each hour for 6 hours. Even though the number of PMNs was significantly reduced in the animals treated with antineutrophil serum, capillary perfusion was not changed compared with controls. These results demonstrate that depleting circulating PMNs does not protect capillary perfusion in our model. These findings suggest that reduced capillary perfusion downstream from an anastomotic repair is not mediated by the presence of PMNs in the microcirculation.
毛细血管灌注受损可能导致皮瓣坏死。血小板栓子、多形核白细胞（PMN）和/或血管痉挛已被确定为可能的原因。本研究调查了PMN在游离皮瓣模型中导致毛细血管灌注受损的作用。使用抗中性粒细胞血清使PMN浓度降低。将20只Sprague-Dawley大鼠的提睾肌分离在单一神经血管蒂上，在模拟技术欠佳的上游动脉吻合和再灌注后，每小时测量毛细血管灌注，持续6小时。尽管用抗中性粒细胞血清处理的动物体内PMN数量显著减少，但与对照组相比，毛细血管灌注并未改变。这些结果表明，在我们的模型中，减少循环中的PMN并不能保护毛细血管灌注。这些发现提示，吻合口修复下游的毛细血管灌注减少并非由微循环中PMN的存在介导。
