Textbook - BIOLOGICAL CHEMISTRY - Gubsky Yu.I. - 2000

Chapter VI. BIOCHEMISTRY OF PHYSIOLOGICAL FUNCTIONS AND SPECIALIZED TISSUES

CHAPTER 29. BIOCHEMISTRY OF BLOOD COAGULATION AND FIBRINOLYTIC SYSTEMS

Blood Coagulation (clotting) is a PHYSIOLOGICAL AND BIOCHEMICAL process whereby blood loses its fluidity and forms thrombi (blood clots). The ability of blood to coagulate and form thrombi is ensured by the functioning of the blood coagulation (hemocoagulation) system, or the hemostatic system.

29.1. FUNCTIONAL AND BIOCHEMICAL PROPERTIES OF THE HEMOSTATIC SYSTEM

The hemostatic system consists of Enzymes and auxiliary Biochemical Factors of Blood Plasma, platelets, and the vascular intima. Under normal physiological conditions, thrombus formation occurs upon vascular wall injury and serves a protective role, preventing blood loss from the circulatory bed. Intravascular thrombus formation (thrombosis) is a pathological process associated with severe disruptions in the Regulation of the hemostatic system.

Structurally, a thrombus is a formation consisting of a meshwork of insoluble fibrin protein fibers with Blood Cells immobilized within the fibrin network. A distinction is made between: white thrombi, composed predominantly of platelet aggregates; and red thrombi, which contain a significant number of erythrocytes.

The maintenance of blood fluidity within Blood Vessels and the Prevention of intravascular blood clotting are provided by the anticoagulant system of the blood, which comprises numerous anticoagulants. Fibrin clots that may form within vessels are degraded by Enzymes of the fibrinolytic system.

From a physiological perspective, a distinction is made between:

1. Vascular-platelet hemostasis, which is the primary response to microcirculatory vessel injury, mediated by the vascular wall and platelets. Vascular-platelet hemostasis plays a leading role in the Initial Stages of bleeding cessation in microvessels. This type of hemostasis includes:

- reflexive vasoconstriction stimulated by vasoconstrictive compounds released from platelets (serotonin, adrenaline, noradrenaline);

- platelet adhesion at the site of vascular injury. The surface to which platelets attach is the Collagen network of the endothelium and subendothelial basement membrane. This involves the interaction of negative charges on the platelet surface with ε-NH₃⁺ groups of lysyl residues in collagen fibrils;

- platelet aggregation, leading to The formation of a platelet plug. Reversible aggregation, stimulated by ADP, is distinguished from irreversible aggregation, induced by Thrombin, collagen, and Ca²⁺. Platelet aggregation and, consequently, thrombus formation are antagonized by cAMP and cyclooxygenase inhibitors (acetylsalicylic acid and other nonsteroidal anti-inflammatory drugs).

2. Coagulation hemostasis, the final outcome of whose activation is the formation of a fibrin clot that immobilizes blood cells and forms a stable thrombus on the endothelial surface. This process is the primary type of hemostasis during bleeding and is executed through a complex enzymatic mechanism of the BLOOD COAGULATION SYSTEM.