The Second Affiliated Hospital, Shantou University Medical College, Shantou, China.
Department of General Surgery, Shanghai Eastern Hepatobiliary Surgery Hospital, Shanghai, China.
Shock. 2021 Jan 1;55(1):121-127. doi: 10.1097/SHK.0000000000001563.
Our previous study demonstrated the types of platelet dysfunction varied at early stage (∼3 h) in trauma-induced coagulopathy (TIC) caused by different types of injuries. And arachidonic acid (AA)-dependent pathway inhibition in platelet seemed to be specific for TIC caused by multiple injury (MI). The aim of this research was to further study AA-dependent pathway inhibition in platelets in a rat model of TIC caused by MI and to explore its potential mechanisms.
Sprague-Dawley rat model of TIC caused by MI was established. We used thrombelastography with platelet mapping as a measure of platelet function to assess the inhibitory extent of AA-dependent activation pathway. Flow cytometry was used to determine the expression of activation-dependent granular protein P-selectin (CD62P). In addition, the plasma levels of 6-Keto-prostaglandin F1 alpha (6-Keto-PGF1α), Prostaglandin E2, and Thromboxane B2 were assessed by enzyme-linked immuno sorbent assay.
The inhibition rate of AA-dependent pathway after injury was significantly higher than that of control. The maximum amplitude decreased in the MI group, compared with that of control. The percentage of CD62P expression in the MI group was remarkably lower than that of control after AA treatment. The plasma concentrations of 6-Keto-PGF1α and PGE2 increased in the MI group.
Platelets inhibition was observed in TIC caused by MI at early stage after injury, which might be partially attributed to AA-dependent activation pathway dysfunction. The increase of plasma Prostacyclin and PGE2 levels may contribute to the inhibition process.
我们之前的研究表明，不同类型损伤导致的创伤性凝血病（TIC）早期（约 3 小时）血小板功能障碍的类型不同。血小板中花生四烯酸（AA）依赖性途径的抑制似乎对多发性损伤（MI）引起的 TIC 具有特异性。本研究旨在进一步研究 MI 引起的 TIC 大鼠模型中血小板中 AA 依赖性途径的抑制，并探讨其潜在机制。
建立 MI 致 TIC 的 SD 大鼠模型。我们使用血小板图谱血栓弹性图作为血小板功能的测量方法，评估 AA 依赖性激活途径的抑制程度。流式细胞术用于测定激活依赖性颗粒蛋白 P-选择素（CD62P）的表达。此外，通过酶联免疫吸附试验评估血浆 6-酮前列腺素 F1α（6-Keto-PGF1α）、前列腺素 E2 和血栓素 B2 的水平。
损伤后 AA 依赖性途径的抑制率明显高于对照组。MI 组的最大振幅较对照组降低。AA 处理后，MI 组 CD62P 表达的百分比明显低于对照组。MI 组血浆 6-Keto-PGF1α 和 PGE2 浓度升高。
MI 导致的 TIC 在损伤后早期即可观察到血小板抑制，这可能部分归因于 AA 依赖性激活途径功能障碍。血浆前列环素和 PGE2 水平的升高可能有助于抑制过程。
