关键词: Coagulopathy Fibrinogen Heatstroke Organ dysfunction Platelet dysfunction

来  源:   DOI:10.1016/j.thromres.2024.109091

Abstract:
BACKGROUND: Heatstroke is a critical heat-related condition characterized by coagulopathy and multiple organ dysfunction. One of the most severe complications of heatstroke is disseminated intravascular coagulation. This condition manifests as excessive clot formation and bleeding that are primarily due to platelet depletion and dysfunction. Fibrinogen plays a crucial role in hemostasis because it links integrin αIIbβ3 on adjacent platelets, thereby promoting the platelet activation and aggregation necessary for clot formation. However, reduced fibrinogen levels may impair the formation of the initial platelet plug and increase the risk of bleeding. The current study explored the effect of fibrinogen on platelet dysfunction in a heatstroke model.
METHODS: Male Wistar rats were subjected to heat stress, and subsequent changes in hemodynamic, biochemical, and coagulation parameters were analyzed. Platelet viability, aggregation, adhesion, spreading and fibrin clot retraction were assessed.
RESULTS: The rats with heatstroke exhibited a variety of clinical symptoms, including hypotension, tachycardia, multiple organ dysfunction, and coagulopathy. Platelet viability in the heatstroke group was comparable to that in the healthy control group. However, the heatstroke group exhibited significant reductions in plasma fibrinogen levels and platelet aggregation, adhesion, spreading, and fibrin clot retraction. Notably, fibrinogen supplementation markedly augmented the aggregation responses of platelets in the heatstroke group. The impairment of platelet adhesion, spreading, and fibrin clot retraction in the rats with heatstroke was partially ameliorated by fibrinogen supplementation.
CONCLUSIONS: An early use of fibrinogen replacement may serve as a therapeutic intervention to alleviate platelet hyporeactivity and prevent the complications in patients with heatstroke.
摘要:
背景:中暑是一种以凝血障碍和多器官功能障碍为特征的危重热相关疾病。中暑最严重的并发症之一是弥散性血管内凝血。这种情况表现为过度的凝块形成和出血,这主要是由于血小板消耗和功能障碍。纤维蛋白原在止血中起着至关重要的作用,因为它连接了邻近血小板上的整合素αIIbβ3,从而促进凝块形成所必需的血小板活化和聚集。然而,降低的纤维蛋白原水平可能会损害初始血小板栓的形成,并增加出血的风险。本研究探讨了纤维蛋白原对中暑模型中血小板功能障碍的影响。
方法:雄性Wistar大鼠接受热应激,以及随后的血液动力学变化,生物化学,并对凝血参数进行分析。血小板活力,聚合,附着力,评估了扩散和纤维蛋白凝块回缩。
结果:中暑大鼠表现出多种临床症状,包括低血压,心动过速,多器官功能障碍,和凝血病。中暑组的血小板活力与健康对照组相当。然而,中暑组血浆纤维蛋白原水平和血小板聚集显著降低,附着力,传播,和纤维蛋白凝块收缩。值得注意的是,补充纤维蛋白原显著增强中暑组血小板的聚集反应.血小板粘附的损害,传播,补充纤维蛋白原部分改善了中暑大鼠的纤维蛋白凝块回缩。
结论:早期使用纤维蛋白原替代治疗可作为治疗干预措施,以减轻中暑患者的血小板低反应性和预防并发症。
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