Hemostasis and Vascular spasm in animals

Hemostasis and Vascular spasm in animals

Hemostasis

Hemostasis means prevention of blood loss from damaged vessels.

Mechanism of hemostasis-

1. Vascular spasm
2. Formation of platelet plug
3. Blood coagulation and organization of fibrous tissue.

Vascular spasm

Injury or trauma to the blood vessels stimulates reflex constriction of the blood vessels through the sympathetic division or the local myogenic spasm by the action of serotonin (5-hydroxy tryptamine) to close even the large blood vessels to prevent excessive blood loss.

When the injury is severe with extensive tissue damage (Crushing, laceration) this spasm is strong and bleeding is less. Smooth cut causes weak spasm and bleeding is severe.

Formation of Platelet plug

Platelets have contractile proteins, the actin and myosin, factor XIII, the fibrin stabilising factor, enzyme systems for the synthe­sis of cAMP, ATP, ADP and prostaglandins (PGG₂, PGH₂, PG1₂ and PGF₂). Platelets are activated by their contact with collagen, which is present in the subendothelial membrane or by substances like ADP, serotonin and thromboxane A₂ released from damaged cells.

Immediately after the vascular endothelial damage, the subendothelial collagen attracts the platelets to the site of injury. The platelets attach to the injured surface. They then undergo a series of complex physical and biochemical changes like swelling of the plate­lets, projection of radiating processes, (pseudopods) from the platelets and their adherence with the endothelial wall of the blood vessels. Factors vWF and fibronectin from subendothelium and plate­lets help in platelet adhesion.

This reaction in turn stimulates release of Ca⁺⁺ which stimulates the enzyme systems of the platelets and causes the release of ADP and thromboxane-A₂ which activate other platelets resulting in adherence of more number of plate­lets in the damaged endothelial wall forming the platelet plug.

This plugs the injury on the blood vessel and prevents blood loss. Thromboxane-A₂ is the most potent platelet-aggregating agent that lowers platelet cAMP and also causes vasoconstriction. PGG₂ and PGH₂ also cause platelet aggregation, whereas PGI₂ produced by the normal endothelium is a vasodilator which acts as a powerful inhibitor of platelet adhesion / aggregation.

Platelet aggregation is prevented by prostacyclins produced by endothelial cells of the artery and lungs. In normal blood flow, prostacyclin level is more than thromboxane and aggregation is prevented. When arterial walls are damaged, prostacyclin level is reduced and thromboxane level becomes high leading to platelet aggregation.

Blood coagulation or blood clotting

Many substances present in tissue and blood affect coagulation. Substances that promote coagulation are called as procoagulants‚ and those inhibiting coagulation are anticoagulants.

Normally in the blood, anticoagulant activity predominates and blood does not coagulate. But, when a vessel is ruptured, the procoagulants activity in the damaged area becomes more and the blood clots.

Clot is the meshwork of fibrin threads running in all directions to entrap the blood cells, platelets and plasma. This is achieved by the activation of series of clotting factors of the blood by two mechanisms- The intrinsic and Extrinsic systems.