贝塔2-激动剂克伦布托罗尔有助于保持心肌在机械卸载期间恢复的潜力吗?
Hiroshi Tsuneyoshi1, Wnimunk Oriyanhan, Hideo Kanemitsu
1Department of Cardiovascular Surgery, Graduate School of Medicine, Kyoto University, Kyoto, 606-8507, Japan.
Circulation
|September 15, 2005
概括
克伦布托罗尔在卸载过程中没有防止左心室缩,但改善了基因表达和β-上腺反应能力. 慢性使用可能会降低β2-上腺素受体的调节.
科学领域:
- 心血管生理学心血管生理学
- 药理学 药理学是指药理学的学科.
背景情况:
- 慢性机械卸载导致左心室 (LV) 缩,可能会阻碍使用LV辅助设备的恢复.
- 像克伦布特罗尔这样的β2-上腺素受体 (AR) 激动剂可以抵消缩并改善心脏功能.
- 有限的数据存在在LV卸载期间的克伦布特罗尔的影响.
研究的目的:
- 为了研究丁醇对LV缩和卸载过程中的功能的影响.
- 评估克伦布醇对心肌基因表达和亡的影响.
- 在没有负荷的心脏中评估克伦布特罗尔治疗后的β-上腺素反应.
主要方法:
- 在老鼠中进行异型心脏移植以诱导LV卸载.
- 随机分配到克伦布特罗尔治疗 (2 mg/kg/天2周) 或盐水控制.
- 评估 LV 体重,乳头肌肉功能,β-AR响应能力和基因表达 (SERCA2a,MHC,caspase-3,ARs).
主要成果:
- 由于卸载,clenbuterol并没有阻止LV体重减少48%,但增加了宿主心脏重量.
- 在发展的紧张状态上没有差异,但在克伦布醇组中对异二醇的内反应得到了改善.
- 克伦布托罗尔改善了SERCA2a和β-MHC mRNA表达,降低了β2-AR mRNA,并显示了减少caspase-3表达的趋势.
结论:
- 克伦布托罗尔在卸载过程中没有防止LV缩,但增强了基因表达和β-上腺素反应能力.
- 克伦布醇在卸载过程中预防心肌亡的潜力.
- 慢性使用克伦布醇可能导致β2-AR下调.
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