DELAYED TREATMENT EFFECTS OF XANTHINE OXIDASE INHIBITION ON SYSTOLIC OVERLOAD-INDUCED LEFT VENTRICULAR HYPERTROPHY AND DYSFUNCTION

The nonpurine selective xanthine oxidase (XO) inhibitor febuxostat attenuates development of left ventricular (LV) hypertrophy and dysfunction in mice when treatment is initiated within 1 hour of transverse aortic constriction (TAC). This study investigated whether a 7-day delay of treatment with th...

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Detalles Bibliográficos
Autores principales: Xu, X., Zhao, L., Hu, X., Zhang, P., Wessale, J., Bache, R., Chen, Y.
Formato: Texto
Lenguaje:English
Publicado: Taylor & Francis 2010
Materias:
Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2903770/
https://www.ncbi.nlm.nih.gov/pubmed/20544512
http://dx.doi.org/10.1080/15257771003738683
Descripción
Sumario:The nonpurine selective xanthine oxidase (XO) inhibitor febuxostat attenuates development of left ventricular (LV) hypertrophy and dysfunction in mice when treatment is initiated within 1 hour of transverse aortic constriction (TAC). This study investigated whether a 7-day delay of treatment with the XO inhibitors febuxostat or allopurinol would reverse TAC-induced changes after onset of heart failure (HF). Neither treatment significantly affected TAC-induced LV hypertrophy; only febuxostat caused a modest improvement in LV function (∼10% increase in LV ejection fraction). However, the purine analog allopurinol tended to increase mortality compared with vehicle or febuxostat in HF mice.

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