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Anticoagulant Rodenticide Toxicity (view source)
Revision as of 14:13, 23 August 2010
, 14:13, 23 August 2010→Mechanism of Toxicity
Normally, haemostastis is maintained by three key events<sup>4</sup>. 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. Aspects of the latter two stages are dependent on vitamin K and it is these which are influenced by anticoagulant rodenticide activity.
Normally, haemostastis is maintained by three key events<sup>4</sup>. 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. Aspects of the latter two stages are dependent on vitamin K and it is these which are influenced by anticoagulant rodenticide activity.
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).
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).