Effects of ketanserin on hypergranulation tissue formation, infection, and healing of equine lower limb wounds.

The objective of this multicentre, randomized, controlled field study was to determine the efficacy of ketanserin gel in preventing exuberant granulation tissue formation (hypergranulation) and infection in equine lower limb wounds. Horses and ponies (n = 481) with naturally occurring wounds were randomized to either topical treatment with ketanserin gel (n = 242) or a positive control (Belgium, Germany: ethacridin lactate solution, n = 120; France, United Kingdom: malic, benzoic, and salicylic acid [MBS] cream, n = 119). Treatment continued until the wound healed (success), formed hypergranulation tissue (failure), or became infected (failure). Treatment was terminated after 6 months in all remaining animals. Ketanserin was successful in 88% of cases. Wounds treated with ketanserin were 2 and 5 times more likely to heal successfully than were those treated with MBS or ethacridin lactate, respectively. Ketanserin gel is thus more effective than these standard treatments in preventing hypergranulation tissue and infection of equine lower limb wounds.

In vitro studies on the effects of flubendazole against Toxocara canis and Ascaris suum.

Adult Toxocara canis and Ascaris suum were incubated in vitro in media containing 0.1, 1, 10 or 100 micro g/ml flubendazole in order to study drug-derived effects. This incubation was done for 8 h and repeated (in some groups) after 24 h for another 8 h. The onset and intensity of flubendazole-derived effects were dosage-dependent and time-dependent, i.e. the same grade of damage was reached when incubating for a longer period at a low dosage or for a shorter period in medium containing a high amount (10 or 100 micro g/ml) of flubendazole. A repeated incubation in drug-containing medium was superior to a single exposure. Flubendazole is apparently able to penetrate into the worm's interior via the cuticle. This became evident in worms with sealed orifices, which showed identical damage to worms which were not sealed. The type of tissue damage due to flubendazole was identical in both worm species when exposed to any of the drug dosages used. The principal mode of action of flubendazole was based on the complete reduction of microtubuli-polymerisation inside the parasite's cells. This apparently led to the complete destruction of the hypodermis, muscle layer and intestine. Flubendazole also stopped the formation of gametes. Summarising, even low concentrations of flubendazole (0.1 micro g/ml) led to significant and irreversible damage in all worms studied.