Salicylates (NSAID) and cephalosporins presenting the N-methyl-thiotetrazole moiety may reduce the effect of vitamin K1, by inhibition of the vitamin K1 recycling.
No signs of intolerance were displayed at 3 times the therapeutic dose, administered for 3 weeks.
Vitamin K1 is a cofactor necessary for the synthesis of K-dependent coagulation factors (factors II, VII, IX and X). During this synthesis, vitamin K1 is converted into vitamin K1 hydroquinone (active form of vitamin K1) and then into vitamin K1 epoxide. It is then recycled back into vitamin K1. Antivitamin K rodenticides inhibit the recycling of vitamin K1 epoxide, causing a risk of uncontrolled bleeding through the absence of functional factors II, VII, IX and X synthesis. The supply of vitamin K1 must be sufficiently large to activate the alternative hydrogenase enzyme pathway that converts it to its active (hydroquinone) form.
After oral administration, vitamin K1 is rapidly absorbed in the dog.
Some of the vitamin K1 is eliminated with the bile in the intestinal tract after metabolism in the liver, and some is eliminated in urine (in the form of glucuronoconjugated metabolites).