Department of Surgery, University of Cincinnati, Cincinnati, Ohio.
Department of Surgery, University of Cincinnati, Cincinnati, Ohio.
J Surg Res. 2024 Apr;296:643-653. doi: 10.1016/j.jss.2024.01.027. Epub 2024 Feb 14.
Desmopressin (DDAVP) has been utilized clinically in patients taking aspirin (ASA) to improve drug-induced platelet dysfunction. Misoprostol and carboprost, prostaglandin analogs commonly used for postpartum hemorrhage, may also induce platelet aggregation. The aim of this study was to determine the effects of DDAVP, misoprostol, and carboprost administration on platelet aggregability following traumatic brain injury (TBI) in mice treated with ASA.
Male C57BL/6 mice were randomized into seven groups (n = 5 each): untouched, ASA only, Saline/TBI, ASA/TBI, ASA/TBI/DDAVP 0.4 μg/kg, ASA/TBI/misoprostol 1 mg/kg, and ASA/TBI/carboprost 100 μg/kg. TBI was induced via a weight drop model 4-h after ASA (50 mg/kg) gavage. Mice were given an intraperitoneal injection of DDAVP, misoprostol, or carboprost 10 minutes after TBI. In vivo testing was completed utilizing tail vein bleed. Mice were sacrificed 30-min posttreatment and blood was collected via cardiac puncture. Whole blood was analyzed via Multiplate impedance aggregometry, rotational thromboelastometry, and TEG6s.
Mice receiving misoprostol after ASA/TBI demonstrated decreased tail vein bleeding times compared to ASA only treated mice. However, mice treated with misoprostol following ASA and TBI demonstrated decreased platelet aggregability compared to untouched mice and TBI only mice within the arachidonic acid agonist pathway. By contrast, DDAVP and carboprost did not significantly change platelet aggregability via adenosine diphosphate or arachidonic acid following ASA and TBI. However, DDAVP did decrease the platelet contribution to clot via rotational thromboelastometry.
Reversal of medication-induced platelet inhibition has become increasingly controversial after TBI. Based on these results, DDAVP, misoprostol, nor carboprost consistently improve platelet aggregability following TBI in those also treated with ASA.
去氨加压素(DDAVP)已在服用阿司匹林(ASA)的患者中临床用于改善药物诱导的血小板功能障碍。米索前列醇和卡前列素,常用于产后出血的前列腺素类似物,也可能诱导血小板聚集。本研究的目的是确定在接受 ASA 治疗的创伤性脑损伤(TBI)小鼠中,给予 DDAVP、米索前列醇和卡前列素对血小板聚集的影响。
雄性 C57BL/6 小鼠随机分为七组(每组 5 只):未处理、仅 ASA、盐水/TBI、ASA/TBI、ASA/TBI/DDAVP0.4μg/kg、ASA/TBI/米索前列醇 1mg/kg 和 ASA/TBI/卡前列素 100μg/kg。TBI 在 ASA(50mg/kg)灌胃后 4 小时通过落体模型诱导。TBI 后 10 分钟,小鼠给予腹腔内注射 DDAVP、米索前列醇或卡前列素。通过尾静脉出血进行体内检测。治疗后 30 分钟处死小鼠,通过心脏穿刺采集血液。通过 Multiplate 阻抗聚集仪、旋转血栓弹性仪和 TEG6s 分析全血。
ASA/TBI 后接受米索前列醇治疗的小鼠与仅接受 ASA 治疗的小鼠相比,尾静脉出血时间缩短。然而,ASA 和 TBI 后接受米索前列醇治疗的小鼠与未处理小鼠和 TBI 仅小鼠相比,在花生四烯酸激动剂途径中,血小板聚集能力降低。相比之下,ASA 和 TBI 后,DDAVP 和卡前列素通过二磷酸腺苷或花生四烯酸对血小板聚集能力无显著影响。然而,DDAVP 通过旋转血栓弹性仪确实降低了血小板对血栓的贡献。
TBI 后,药物诱导的血小板抑制作用的逆转变得越来越有争议。基于这些结果,在接受 ASA 治疗的 TBI 患者中,DDAVP、米索前列醇和卡前列素均不能一致改善血小板聚集能力。