Lasne Dominique, Jude Brigitte, Susen Sophie
Laboratoire d'hématologie, Hôpital Necker, 149 Rue de Sèvres, 75743 Paris cedex 15, France.
Can J Anaesth. 2006 Jun;53(6 Suppl):S2-11. doi: 10.1007/BF03022247.
To review the evolution of knowledge on physiological hemostasis and the main abnormalities that may interfere with hemostasis in the perioperative period.
Narrative review of the literature, including relevant papers published in English.
Physiological hemostasis controls blood fluidity and rapidly induces hemostatic plug formation in order to stop or limit bleeding. The three distinct phases of the hemostatic process, primary hemostasis, coagulation and fibrinolysis are closely linked to each other and precisely regulated in order to efficiently close vessel wounds, promote vascular healing and maintain vessel patency. Primary hemostasis is the result of complex interactions between the vascular wall, platelets and adhesive proteins. Initiation of the coagulation pathway in vivo is secondary to the exposure of tissue factor (TF) and the formation of TF/VIIa complex which can activate both FIX and FX. This initiation phase is followed by a propagation phase with amplification of thrombin generation. Several control mechanisms exist for localizing fibrin formation to the site of injury including tissue factor pathway inhibitor, protein C system, antithrombin, and glycosaminoglycans on the vessel wall. Fibrinolysis is also a highly regulated system that controls fibrin dissolution. Both constitutive and acquired hemostasic defects exist. The consequences of these abnormalities are highly variable according to the type of defect, and to the genetic and environmental background.
Hemostasis is one of the most complex physiological self-defence systems, not only involved in control of blood fluidity but also interfering in major physiopathological processes. The evolution of our knowledge of the physiology of hemostasis has numerous implications for therapy.
回顾生理性止血知识的演变以及围手术期可能干扰止血的主要异常情况。
对文献进行叙述性综述，包括以英文发表的相关论文。
生理性止血控制血液流动性，并迅速诱导止血栓形成以止血或限制出血。止血过程的三个不同阶段，即初级止血、凝血和纤维蛋白溶解，相互紧密联系并受到精确调节，以有效闭合血管伤口、促进血管愈合并维持血管通畅。初级止血是血管壁、血小板和黏附蛋白之间复杂相互作用的结果。体内凝血途径的启动继发于组织因子（TF）的暴露以及TF/VIIa复合物的形成，该复合物可激活FIX和FX。此启动阶段之后是凝血酶生成放大的传播阶段。存在多种将纤维蛋白形成局限于损伤部位的控制机制，包括组织因子途径抑制物、蛋白C系统、抗凝血酶以及血管壁上的糖胺聚糖。纤维蛋白溶解也是一个高度调节的系统，控制纤维蛋白溶解。存在先天性和获得性止血缺陷。这些异常的后果因缺陷类型以及遗传和环境背景而异。
止血是最复杂的生理自我防御系统之一，不仅参与控制血液流动性，还干扰主要的生理病理过程。我们对止血生理学知识的演变对治疗有诸多影响。
