Andresen D M, O'Shaughnessy M, Acland R D, Anderson G L, Schuscke D, Banis J, Barker J H
Institute of Experimental Clinical Research, Aarhus University Hospital, Skejby, Denmark.
Microsurgery. 1994;15(6):413-20. doi: 10.1002/micr.1920150609.
A common cause of free flap and replant failure is thrombotic occlusion of the anastomosed pedicle vessel(s). Clinical observations and subsequent experimental studies showed that platelet emboli generated at the arterial anastomosis caused significant alterations in the downstream microcirculation. To study both the thrombogenic arterial (anastomosis) site and the downstream microcirculation, we developed an animal model (the isolated rat cremaster) in which we could directly view and quantitatively analyze thrombus formation and the appearance of emboli in the downstream microcirculation. Using this model we studied the effect that reducing blood flow across the arterial anastomotic site had on thrombus formation at the anastomotic site and the appearance of emboli in the downstream microcirculation. In 40 male Sprague-Dawley rats we found that reducing blood flow velocity to approximately half of normal during reperfusion nearly eliminated emboli appearing in the downstream microcirculation compared with controls, 43.9 +/- 31.5 vs. 259.5 +/- 117.8 emboli, respectively. We also found that the same low flow had no effect on thrombus size at the pedicle artery injury site yet significantly decreased the rate at which thrombus formation occurred (time to maximum thrombus size; low flow = 25.3 +/- 8 minutes, normal flow = 6.6 +/- 3 minutes). From these studies we conclude that reducing pedicle artery blood flow in our rat model during reperfusion can protect the down-stream microcirculation from platelet emboli-induced injury; however, the same reduction in flow does not affect thrombus formation in the pedicle artery. Further studies using direct observation/measurement techniques are needed for a better understanding of the mechanisms regulating free flap and replant failure.
游离皮瓣和再植失败的一个常见原因是吻合蒂血管的血栓形成性闭塞。临床观察及后续实验研究表明，动脉吻合处产生的血小板栓子会导致下游微循环发生显著改变。为了研究血栓形成性动脉（吻合）部位及下游微循环，我们建立了一种动物模型（大鼠离体提睾肌），在此模型中我们能够直接观察并定量分析血栓形成情况以及下游微循环中栓子的出现情况。利用该模型，我们研究了降低流经动脉吻合部位的血流对吻合部位血栓形成及下游微循环中栓子出现情况的影响。在40只雄性Sprague-Dawley大鼠中，我们发现，与对照组相比，再灌注期间将血流速度降至正常速度的大约一半时，下游微循环中出现的栓子几乎消失，分别为43.9±31.5个栓子和259.5±117.8个栓子。我们还发现，同样的低血流对蒂动脉损伤部位的血栓大小没有影响，但显著降低了血栓形成的速率（达到最大血栓大小的时间；低血流组 = 25.3±8分钟，正常血流组 = 6.6±3分钟）。从这些研究中我们得出结论，在我们的大鼠模型中，再灌注期间降低蒂动脉血流可保护下游微循环免受血小板栓子诱导的损伤；然而，同样的血流降低并不影响蒂动脉中的血栓形成。需要使用直接观察/测量技术进行进一步研究，以更好地理解调节游离皮瓣和再植失败的机制。
