Krag Andreas Engel, Hvas Christine Lodberg, Kiil Birgitte Jul, Eschen Gete Toft, Damsgaard Tine Engberg, Hvas Anne-Mette
Department of Clinical Biochemistry, Center for Hemophilia and Thrombosis, Aarhus University Hospital, Aarhus, Denmark.
Department of Plastic and Breast Surgery, Aarhus University Hospital, Aarhus, Denmark.
Microsurgery. 2018 Sep;38(6):690-697. doi: 10.1002/micr.30287. Epub 2018 Jan 8.
Remote ischemic conditioning (RIC) administered by non-lethal periods of extremity ischemia and reperfusion attenuates ischemia-reperfusion injury. We aimed to investigate the local and systemic coagulation marker response to flap ischemia-reperfusion injury, and the effects of RIC on coagulation markers following flap ischemia-reperfusion injury.
A musculocutaneous latissimus dorsi flap was subjected to 4 h of ischemia followed by 7 h of reperfusion in 16 female Danish Landrace pigs (39 kg). Systemic venous blood samples were collected 1 h before flap reperfusion. Flap and systemic venous blood samples were collected at reperfusion and hourly during reperfusion. We measured thrombin generation, fibrinogen, von Willebrand factor, antithrombin, thrombin-antithrombin complex, activated partial thromboplastin time (aPTT), and prothrombin time (PT). RIC was performed 1 h before flap reperfusion in the intervention group by three 10-min periods of hind limb ischemia and reperfusion (n = 8). RIC was not performed in the control group (n = 8).
Local and systemic coagulation marker changes were comparable following flap ischemia-reperfusion injury. Flap ischemia-reperfusion injury reduced thrombin generation lag time from 2.0 ± 0.3 to 1.6 ± 0.3 min (P < .001), time-to-peak thrombin from 3.5 ± 0.3 to 3.0 ± 0.5 min (P = .001), peak thrombin from 79.6 ± 8.1 to 74.5 ± 7.1 nM (P = .033), endogenous thrombin potential from 211 ± 24 to 197 ± 19 nM × min (P = .01), antithrombin from 0.91 ± 0.07 to 0.79 ± 0.06 10 IU/l (P = .002), and aPTT from 37 ± 21 to 21 ± 9 s (P = .017). RIC increased peak thrombin (P < .001), endogenous thrombin potential (P < .001), and aPTT (P = .019).
The local coagulation marker response to musculocutaneous flap ischemia-reperfusion could be measured systemically by moderate hypercoagulation. RIC did not substantially influence coagulation markers following musculocutaneous flap ischemia-reperfusion injury.
通过非致死性的肢体缺血和再灌注进行远程缺血预处理(RIC)可减轻缺血再灌注损伤。我们旨在研究皮瓣缺血再灌注损伤后局部和全身凝血标志物的反应,以及RIC对皮瓣缺血再灌注损伤后凝血标志物的影响。
对16只丹麦长白猪(体重39千克)的背阔肌肌皮瓣进行4小时缺血,随后进行7小时再灌注。在皮瓣再灌注前1小时采集全身静脉血样本。在再灌注时及再灌注期间每小时采集皮瓣和全身静脉血样本。我们检测了凝血酶生成、纤维蛋白原、血管性血友病因子、抗凝血酶、凝血酶 - 抗凝血酶复合物、活化部分凝血活酶时间(aPTT)和凝血酶原时间(PT)。干预组在皮瓣再灌注前1小时通过后肢三次10分钟的缺血和再灌注进行RIC(n = 8)。对照组(n = 8)未进行RIC。
皮瓣缺血再灌注损伤后局部和全身凝血标志物变化具有可比性。皮瓣缺血再灌注损伤使凝血酶生成延迟时间从2.0±0.3分钟缩短至1.6±0.3分钟(P <.001),凝血酶达到峰值时间从3.5±0.3分钟缩短至3.0±0.5分钟(P =.001),凝血酶峰值从79.6±8.1纳摩尔降至74.5±7.1纳摩尔(P =.033),内源性凝血酶潜力从211±24纳摩尔·分钟降至197±19纳摩尔·分钟(P =.01),抗凝血酶从0.91±0.07降至0.79±0.06 10国际单位/升(P =.002),aPTT从37±21秒降至21±9秒(P =.017)。RIC增加了凝血酶峰值(P <.001)、内源性凝血酶潜力(P <.001)和aPTT(P =.019)。
皮瓣缺血再灌注损伤后局部凝血标志物的反应可通过中度高凝状态进行全身测量。RIC对肌皮瓣缺血再灌注损伤后的凝血标志物没有实质性影响。