1Department of Anesthesia and Intensive Care Medicine, Medical University InnsbruckInnsbruckAustria. 2Department of Bioengineering, University of California, San Diego (UCSD)La JollaCA. 3Clinical Department of General and Surgical Intensive Care Medicine, Medical University InnsbruckInnsbruckAustria.
Crit Care Med. 2013 Nov;41(11):e301-8. doi: 10.1097/CCM.0b013e31828a4520.
Dilutional coagulopathy after resuscitation with crystalloids/colloids clinically often appears as diffuse microvascular bleeding. Administration of fibrinogen reduces bleeding and increases maximum clot firmness, measured by thromboelastometry. Study objective was to implement a model where microvascular bleeding can be directly assessed by visualizing clot formation in microvessels, and correlations can be made to thromboelastometry.
Randomized animal study.
University research laboratory.
Male Syrian Golden hamsters.
Microvessels of Syrian Golden hamsters fitted with a dorsal window chamber were studied using videomicroscopy. After 50% hemorrhage followed by 1 hour of hypovolemia resuscitation with 35% of blood volume using a high-molecular-weight hydroxyethyl starch solution (Hextend, Hospira, MW 670 kD) occurred. Animals were then treated with 250 mg/kg fibrinogen IV (Laboratoire français du Fractionnement et des Biotechnologies, Paris, France) or an equal volume of saline before venular vessel wall injuries was made by directed laser irradiation, and the ability of microthrombus formation was assessed.
Thromboelastometric measurements of maximum clot firmness were performed at the beginning and at the end of the experiment. Resuscitation with hydroxyethyl starch and sham treatment significantly decreased FIBTEM maximum clot firmness from 32 ± 9 mm at baseline versus 13 ± 5 mm after sham treatment (p < 0.001). Infusion of fibrinogen concentrate significantly increased maximum clot firmness, restoring baseline levels (baseline 32 ± 9 mm; after fibrinogen administration 29 ± 2 mm). In vivo microthrombus formation in laser-injured vessels significantly increased in fibrinogen-treated animals compared with sham (77% vs 18%).
Fibrinogen treatment leads to increased clot firmness in dilutional coagulopathy as measured with thromboelastometry. At the microvascular level, this increased clot strength corresponds to an increased prevalence of thrombus formation in vessels injured by focused laser irradiation.
晶体/胶体复苏后出现的稀释性凝血病在临床上常表现为弥漫性微血管出血。纤维蛋白原的输注可减少出血并增加血栓弹力描记法测量的最大血凝块硬度。本研究旨在建立一种模型，通过可视化微血管中的血栓形成直接评估微血管出血，并与血栓弹力描记法相关联。
随机动物研究。
大学研究实验室。
雄性叙利亚金黄仓鼠。
使用视频显微镜研究叙利亚金黄仓鼠的微血管，在发生 50%出血后，通过输注相当于 35%血容量的高分子量羟乙基淀粉溶液（Hextend，Hospira，MW 670 kD）进行 1 小时的低血容量复苏。然后，在静脉小血管壁损伤前，用 250 mg/kg 纤维蛋白原 IV（Laboratoire français du Fractionnement et des Biotechnologies，Paris，France）或等量生理盐水处理动物，并评估微血栓形成的能力。
在实验开始和结束时进行血栓弹力描记法测量最大血凝块硬度。羟乙基淀粉复苏和假处理显著降低了 FIBTEM 最大血凝块硬度，从基线的 32 ± 9 mm 降至假处理后的 13 ± 5 mm（p < 0.001）。纤维蛋白原浓缩物的输注显著增加了最大血凝块硬度，恢复了基线水平（基线 32 ± 9 mm；纤维蛋白原给药后 29 ± 2 mm）。与假处理相比，在纤维蛋白原处理的动物中，激光损伤血管中的体内微血栓形成明显增加（77%比 18%）。
纤维蛋白原治疗可导致血栓弹力描记法测量的稀释性凝血病中血凝块硬度增加。在微血管水平，这种增加的血凝块强度与聚焦激光照射损伤的血管中血栓形成的发生率增加相对应。
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