凝血不平衡在实验性腹膜炎系统性疾病形成中的作用

V. Gutsulyuk, I. V. Savуtskyi
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引用次数: 0

摘要

背景今天,腹膜炎仍然是腹部手术和理论病理生理学中最困难的问题之一。腹膜炎的主要发病机制之一是止血系统紊乱和播散性血管综合征的发展。传播性血管综合征引起的微循环障碍会导致组织缺氧,从而导致器官和身体系统功能障碍。目的:研究大鼠实验性粪性腹膜炎条件下血小板及凝血止血的变化。材料和方法。对24只非线性实验室大鼠进行了实验研究,将其分为2组:1组-完整对照(动物接受蒸馏水),2组-对照病理组动物。根据《药物临床前研究方法学建议》,在V.A.Lazarenko模型上研究了实验性腹膜炎。根据公认的方法测定血管血小板和凝血止血指标。后果在实验性腹膜炎的第一天,观察到凝血速率急剧增加,血小板的质量特性发生变化,影响了它们的聚集能力和已经形成的血块的回缩。在实验的第4天,建立了血管-血小板连接的变化,表明由于凝血时间、血小板聚集能力和血栓回缩的减少,血小板的潜力已经耗尽,而血小板的数量可能增加,现在可能有时间从储存库“进入”血液。在实验性粪便腹膜炎的背景下,凝血-止血系统的变化表明,在第一天就已经出现了高凝状态,取而代之的是低凝状态,这表明凝血潜力的酶系统已经耗尽(最早在第4天),这种情况一直持续到实验结束。结论在粪便腹膜炎止血系统紊乱的发展过程中,关键作用属于凝血系统激活的内部和外部机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
STUDY OF THE ROLE OF HEMOCOAGULATION DISBALANCE AS A KEY PATHOGENETIC PREDICTORS IN THE FORMATION OF SYSTEMIC DISORDERS IN EXPERIMENTAL PERITONITIS
Background. Peritonitis today continues to be one of the most difficult problems of both abdominal surgery and theoretical pathophysiology. One of the leading pathogenetic mechanisms of peritonitis is disorders in the hemostasis system and the development of dissemination vascular syndrome. Blockade of microcirculation caused by the development of dissemination vascular syndrome leads to tissue hypoxia and, as a result, to dysfunction of organs and body systems. Aim: is to study changes in vascular-platelet and coagulation hemostasis under conditions of experimental fecal peritonitis in rats. Materials and methods. Experimental studies were conducted on 24 non-linear laboratory rats, which were divided into 2 groups: 1 group – intact control (animals received distilled water), 2 group – animals of the control pathology group. According to the "Methodological recommendations for preclinical study of medicinal products", experimental peritonitis was studied on the model of V. A. Lazarenko. Indicators of vascular-platelet and coagulation hemostasis were determined according to generally accepted methods. Results. On the first day of experimental peritonitis, a sharp increase in the rate of blood clotting and changes in the quality properties of platelets were noted, affecting their aggregation ability and retraction of an already formed blood clot. On the 4th day of the experiment, changes in the vascular-platelet link were established, indicating the exhaustion of the platelet potential, due to a decrease in blood clotting time, platelet aggregation ability, and blood clot retraction against the background of a probable increase in the number of blood platelets, which probably by now had time "get" to the bloodstream from the depot. Changes in the coagulation hemostasis system against the background of experimental fecal peritonitis indicate the development of hypercoagulation already on the first day, which is replaced by a hypocoagulation state, which indicates the exhaustion of the enzymatic systems of blood coagulation potential (as early as on the 4th day), which lasted until the end of the experiment. Conclusion. In the development of disorders of the hemostasis system in fecal peritonitis, the key role belongs to both the internal and external mechanisms of activation of the blood coagulation system.
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