HAEMOSTASIS AND MECHANISM OF HAEMOSTASIS

Haemostasis

Hemostasis is the arrest of blood flow and control of haemorrhage from an injured blood vessel. It is the process by which the blood is retained within the vascular system. Haemostasis is initiated when a blood vessel is injured. The mechanism of haemostasis is very complex and involves platelets, the coagulation factors and fibrinolytic system.

MECHANISM OF HAEMOSTASIS

Haemostasis involves a series of delicately balanced physical and biochemical changes following an injury to a blood vessel (Fig. 7.1(a)). As the most immediate response, the blood vessel constricts reducing the volume of blood flowing out. The platelets aggregate at the site of the injury and form a plug which further reduces the bleeding. These activated platelets secrete substances that initiate the coagulation factors. The factors interact serially, forming a fibrin-network or clot in which white cells, red cells and platelets are enmeshed and form a solid plug of blood (coagulation) which seals off the injury completely. Slow lysis of the clot, fibrinolysis, then begins and the site of injury is finally repaired

The entire mechanism of haemostasis can be divided into three parts:

1. Extravascular effects 

2. Vascular effects

Extravascular Effects

The extravascular effects can be physical or biochemical. The physical effects include the attempts of the tissue surrounding the injury site (muscle, skin etc) to mechanically close the break in the blood vessel. Certain substances are released from the tissues which react with the plasma and platelet factors in the process of coagulation. These substances are responsible for the extravascular biochemical effects. 

Vascular Effects

The blood vessels themselves participate in haemostasis in two ways. 

Vasoconstriction Blood vessels constrict almost instantaneously when injured. This spontaneous response is then prolonged by serotonin, a substance secreted by platelets. 

Platelet plug Blood vessels are internally lined by a single layer of epithelial cells, called endothelium. If this endothelium is disrupted due to trauma, the underlying basement membrane containing collagen fibres is exposed. When platelets circulating in the blood come in contact with the collagen, they immediately adhere to the wall at the site of injury. The platelets then release adenosine diphosphate (ADP) which promotes the adhesion and aggregation of platelets until a haemostatic plug covers the site of injury. Platelets also produce serotinin for vasoconstriction and platelets factor 3 (PF3) which participates in coagulation. 

 

Intravascular effects in an extremely complex sequence of reactions, intravascular factors produce a firm clot from liquid blood. This process, initiated by platelets, is followed by activation of the intrinsic system of coagulation from the substances present within the blood. A fibrin clot is then formed as a result of coagulation.