Delayed treatment effects of xanthine oxidase inhibition on systolic overload-induced left ventricular hypertrophy and dysfunction.
Delayed treatment effects of xanthine oxidase inhibition on systolic overload-induced left ventricular hypertrophy and dysfunction.
复制标题
黄嘌呤氧化酶抑制对收缩期超负荷引起的左心室肥厚和功能障碍的延迟治疗效果。
DOI：
10.1080/15257771003738683
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发表时间：
2010
期刊：
影响因子：
--
通讯作者：
Chen,Y
中科院分区：
文献类型：
--
作者：
Xu,X;Zhao,L;Hu,X;Zhang,P;Wessale,J;Bache,R;Chen,Y
当在主动脉横缩窄（TAC）1小时内开始治疗时，非嘌呤选择性黄嘌呤氧化酶（XO）抑制剂非布司他可减轻小鼠左心室（LV）肥大和功能障碍的发展。本研究调查了XO抑制剂非布司他或别嘌呤醇治疗延迟7天是否会逆转心力衰竭（HF）发作后TAC诱导的变化。两种治疗均未显著影响TAC诱导的LV肥大;仅非布司他引起LV功能适度改善（LV射血分数增加约10%）。然而，与溶媒或非布司他相比，嘌呤类似物别嘌呤醇倾向于增加HF小鼠的死亡率。
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.