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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11294256 | PMC |
| http://dx.doi.org/10.1007/s43440-024-00617-1 | DOI Listing |
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In recent years, a global increase in allergy incidence following chemical exposure has been observed. While the process of skin sensitization is well characterized through the adverse outcome pathway (AOP) framework, the immunological mechanisms underlying respiratory sensitization remain less well understood. Respiratory sensitizers are classified as substances of very high concern (SVHC) under the European Union (EU) regulation for the registration, evaluation, authorization and restriction of chemicals (REACH), emphasizing the importance of evaluating respiratory tract sensitization as a critical hazard.
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Thromboxane A (TXA), a prothrombotic factor that induces platelet aggregation and thrombosis, acts as a vasoconstrictor by activating TXA receptors (TP receptors). TXA is extremely unstable and metabolizes into three major metabolites: 2,3-dinor thromboxane B (2,3-dinor-TXB), 11-dehydro TXB(11-dh-TXB), and 11-dehydro-2,3-dinor TXB(11-dh-2,3-dinor-TXB). 8-Iso-prostaglandin F(8-iso-PGF), a prostaglandin-like compound widely considered the best biomarker of oxidative stress, can also activate TP receptors.
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Pimobendan oral solution is bioequivalent to pimobendan chewable tablets in beagle dogs.
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