RESUMO
Oclacitinib is an oral therapy indicated for pruritus associated with allergic or atopic dermatitis in dogs. This study sought to assess pet owners' perceptions of the relative convenience and value of the conventional film-coated formulation and the chewable formulation. A quantitative discrete-choice experimental methodology was applied, comparing (conventional, film-coated) oclacitinib versus chewable oclacitinib using unbranded treatment profiles. Initially, a qualitative interview phase with pet owners and veterinarians was conducted to develop detailed treatment profiles. Subsequently, pet owners participated in a quantitative survey. Overall, 1590 pet owners provided survey responses. Most respondents (62%) reported having experienced challenges administering tablet-based therapies to their dog(s). Half of all respondents (52%) had experience administering flavoured or chewable tablets to their dog. Comparing oclacitinib and chewable oclacitinib (with or without associated costs), the majority of the respondents preferred the chewable formulation in all regions across short-term and long-term scenarios (≥58%; all p < 0.05). The current research is one of few survey-driven studies for treatment preferences in companion animal medicine. Veterinarians may offer chewable or palatable treatment options where available, with potential positive impacts on convenience, compliance, outcomes, quality of life, and the human-animal bond.
RESUMO
The vascular resting tone of the porcine basilar artery appears to be mostly maintained by a balance between spontaneously released nitric oxide (NO) from endothelial cells and thromboxane (TX) A(2) from endothelial and smooth muscle cells. However the precise role of the interaction between the above two substances in the control of vascular tone is unclear. We attempted to clarify the interaction between NO and TXA(2) using cultured porcine basilar arterial endothelial cells. The cultured endothelial cells produced NO spontaneously, while TXB(2) (a stable metabolite of TXA(2)) production remained below the detection limit. Ibuprofen (a COX inhibitor) and ozagrel (a TXA(2) synthetase inhibitor) significantly increased the spontaneous production of NO, which was not affected by 1400W (an iNOS inhibitor). l-Nitro arginine (a NOS inhibitor) significantly induced TXB(2) production. These results suggest that NO may inhibit COX or TXA(2) synthetase, and that therefore inhibition of NOS might disinhibit COX or TXA(2) synthetase, subsequently inducing TXA(2) production. On the other hand, as TXA(2) and other contractility-related prostaglandin(s) may inhibit NOS, therefore the inhibition of COX or TXA(2) synthetase might disinhibit NOS, and then increase the spontaneous production of NO in porcine basilar arterial endothelial cells.