卡维地洛调节低氧诱导factor-1alpha和血管内皮生长因子的表达在容量超负荷心衰大鼠模型。
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害羞的公斤来说,陆MJ, Chang H,太阳,为什么王BW, Kuan P
卡维地洛调节低氧诱导factor-1alpha和血管内皮生长因子的表达在容量超负荷心衰大鼠模型。
J卡失败。2005年3月,11 (2):152 - 9。
- PubMed ID
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15732037 (在PubMed]
- 文摘
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背景:β受体阻断剂的使用已成为一种有益的治疗充血性心力衰竭。低氧factor-1alpha (HIF-1alpha)心室心肌的严格监管。然而,HIF-1alpha的表达在慢性心力衰竭造成过载和体积与β受体阻滞剂治疗后却鲜为人知。方法和结果:为了测试假设HIF-1alpha在失败的过程中发挥作用心肌由于容量超负荷,创建一个aorta-caval分流为成人Sprague-Dawley 4周大鼠诱发容量超负荷心力衰竭。卡维地洛在手术后50毫克/公斤体重/天。心脏重量和体重比率从2.6 + / - 0.3增加虚假的组为3.9 + / - 0.7分流组(P <措施)。左心室舒张末期尺寸从6.5 + / - 0.5毫米增加到8.7 + / - 0.6毫米(P <措施)。用卡维地洛治疗分流组逆转心脏重量和心室维基线值。免疫印迹显示HIF-1alpha,血管内皮生长因子(VEGF)和脑利钠肽(BNP)蛋白是调节和神经生长因子(NGF-beta)分流组中表达下调。实时聚合酶链反应显示,信使rna的HIF-1alpha, VEGF,法国巴黎增加和mRNA NGF-beta减少分流组。 Treatment with carvedilol reversed both protein and mRNA of HIF-1alpha, VEGF, BNP, and NGF-beta to the baseline values. Increased immunohistochemical labeling of HIF-1alpha, VEGF, and BNP in the ventricular myocardium was observed in the shunt group and carvedilol again normalized the labeling. CONCLUSION: HIF-1alpha and VEGF mRNA and protein expression were upregulated in the rat model of volume-overload heart failure. Treatment with carvedilol is associated with a reversal of abnormal regulation of HIF-1alpha and VEGF in the failing ventricular myocardium.