From the *NISCHR Haemostasis Biomedical Research Unit, Morriston Hospital, Abertawe Bro Morgannwg University Health Board, Swansea, Wales, United Kingdom; †College of Medicine, Swansea University, Swansea, Wales, United Kingdom; ‡The Welsh Centre for Burns and Plastic Surgery, Morriston Hospital, Swansea, Wales, United Kingdom; §Emergency Department, Morriston Hospital, Abertawe Bro Morgannwg University Health Board, Swansea, Wales, United Kingdom; ‖School of Health Science, Cardiff Metropolitan University, Cardiff, Wales, United Kingdom; and ¶College of Engineering, Swansea University, Swansea, Wales, United Kingdom.
Anesth Analg. 2016 Jan;122(1):21-6. doi: 10.1213/ANE.0000000000000992.
Anesthesia, critical illness, and trauma are known to alter thermoregulation, which can potentially affect coagulation and clinical outcome. This in vitro preclinical study explores the relationship between temperature change and hemostasis using a recently validated viscoelastic technique. We hypothesize that temperature change will cause significant alterations in the microstructural properties of clot.
We used a novel viscoelastic technique to identify the gel point of the blood. The gel point identifies the transition of the blood from a viscoelastic liquid to a viscoelastic solid state. Furthermore, identification of the gel point provides 3 related biomarkers: the elastic modulus at the gel point, which is a measure of clot elasticity; the time to the gel point (TGP), which is a measure of the time required to form the clot; and the fractal dimension of the clot at the gel point, df, which quantifies the microstructure of the clot. The gel point measurements were performed in vitro on whole blood samples from 136 healthy volunteers over a temperature range of 27°C to 43°C.
There was a significant negative correlation between increases in temperature, from 27°C to 43°C, and TGP (r = -0.641, P < 0.0005). Conversely, significant positive correlations were observed for both the elastic modulus at the gel point (r = 0.513, P = 0.0008) and df (r = 0.777, P < 0.0005) across the range of 27°C to 43°C. When temperature was reduced below 37°C, significant reductions in df and TGP occurred at ≤32°C (Bonferroni-corrected P = 0.0093) and ≤29°C (Bonferroni-corrected P = 0.0317), respectively. No significant changes were observed when temperature was increased to >37°C.
This study demonstrates that the gel point technique can identify alterations in clot microstructure because of changes in temperature. This was demonstrated in slower-forming clots with less structural complexity as temperature is decreased. We also found that significant changes in clot microstructure occurred when the temperature was ≤32°C.
麻醉、危重病和创伤已知会改变体温调节，这可能会影响凝血和临床结果。这项体外临床前研究使用最近验证的黏弹性技术探索了温度变化与止血之间的关系。我们假设温度变化会导致血栓微观结构特性发生显著改变。
我们使用一种新的黏弹性技术来确定血液的凝胶点。凝胶点确定血液从黏弹性液体向黏弹性固体状态的转变。此外，凝胶点的确定提供了 3 个相关的生物标志物：凝胶点处的弹性模量，它是血栓弹性的度量；达到凝胶点的时间（TGP），它是形成血栓所需的时间的度量；以及凝胶点处血栓的分形维数 df，它量化了血栓的微观结构。在 27°C 至 43°C 的温度范围内，对来自 136 名健康志愿者的全血样本进行了体外凝胶点测量。
从 27°C 升高到 43°C，温度升高与 TGP 呈显著负相关（r = -0.641，P < 0.0005）。相反，在 27°C 至 43°C 的范围内，凝胶点处的弹性模量（r = 0.513，P = 0.0008）和 df（r = 0.777，P < 0.0005）均呈显著正相关。当温度降至 37°C 以下时，在≤32°C（经 Bonferroni 校正的 P = 0.0093）和≤29°C（经 Bonferroni 校正的 P = 0.0317）时，df 和 TGP 显著降低。当温度升高到>37°C 时，未观察到显著变化。
这项研究表明，凝胶点技术可以识别由于温度变化导致的血栓微观结构改变。当温度降低时，这种情况在形成较慢、结构较简单的血栓中表现更为明显。我们还发现，当温度≤32°C 时，血栓微观结构发生显著变化。
