Changes

Normally, haemostastis is maintained by three key events⁴. Firstly, platelets are activated, adhere to endothelial connective tissue and aggregate to form a platelet plug. Next, substances are released that trigger coagulation and vasoconstriction. Finally, fibrinogen is polymerised to fibrin which reinforces the platelet plug. Some components of the coagulation and fibrin formation stages are dependent on vitamin K, and it is these which are influenced by anticoagulant rodenticide activity.

Normally, haemostastis is maintained by three key events⁴. Firstly, platelets are activated, adhere to endothelial connective tissue and aggregate to form a platelet plug. Next, substances are released that trigger coagulation and vasoconstriction. Finally, fibrinogen is polymerised to fibrin which reinforces the platelet plug. Some components of the coagulation and fibrin formation stages are dependent on vitamin K, and it is these which are influenced by anticoagulant rodenticide activity.

 

Two simultaneous cascades are activated to achieve coagulation: the intrinsic and extrinsic pathways. These converge at the common pathway, which eventually results in the formation of fibrin from fibrinogen. The factors involved in the intrinsic pathway are

When the coagulation mechanism is set into motion, 2 separate "pathways" are simultaneously set into operation to effect hemostasis. The "intrinsic route" refers to a relatively slow process (lasting 5 - 15 minutes, in vitro), while the "extrinsic route" is a relatively rapid one (lasting 10 - 12 seconds), following contact between blood and damaged tissue. Following activation, both routes operate independently and eventually converge at the "common pathway." At this convergence, a single route (common coagulation pathway) is followed which eventually causes the soluble plasma protein, fibrinogen, to be converted into the insoluble fibrin (see Circulation diagram below).

Within each independent (intrinsic, extrinsic) pathway and in the common pathway, at least one coagulation (clotting) factor that depends on the action of vitamin K for its synthesis is involved. When vitamin K is deficient or inhibited, the flow of the cascade is interrupted, preventing eventual formation of the insoluble fibrin polymer.

Within each independent (intrinsic, extrinsic) pathway and in the common pathway, at least one coagulation (clotting) factor that depends on the action of vitamin K for its synthesis is involved. When vitamin K is deficient or inhibited, the flow of the cascade is interrupted, preventing eventual formation of the insoluble fibrin polymer.