在实验性心力衰竭中,simvastatin使自主神经控制正常化
Rainer U Pliquett1, Kurtis G Cornish, Jacob D Peuler
1Department of Physiology and Biophysics, University of Nebraska Medical Center, Omaha, NE 68198-4575, USA.
Circulation
|April 16, 2003
概括
像simvastatin一样,他类药物可以通过正常化交感神经系统活动和巴罗反射功能来改善慢性心力衰竭 (CHF),独立于它们的降脂作用. 这意味着一种新的治疗方法来治疗心血管疾病.
科学领域:
- 心血管生理学心血管生理学
- 药理学 药理学 是一个学科.
- 自主神经科学 自主神经科学
背景情况:
- 类他类药物 (HMG-CoA减少酶抑制剂) 在慢性心力衰竭 (CHF) 中显示有好处.
- 类药物对CHF自主功能的影响尚未完全理解.
- 自主功能障碍,包括交感性多动性,是心血管衰竭的标志.
研究的目的:
- 在CHF的子模型中研究simvastatin对自主功能的影响.
- 评估simvastatin是否影响交感神经活动和巴罗反射灵敏度.
- 要确定这些效应是否独立于降脂性质.
主要方法:
- 慢性心力衰竭 (CHF) 在子中通过心室节奏诱导.
- 子接受了载体或simvastatin (低剂量或高剂量).
- 在有意识的动物中测量了性交感神经活动 (RSNA),血上诺亚上腺素和巴罗反射功能.
主要成果:
- 基线RSNA和北上腺素水平在CHF子中升高.
- 高剂量的simvastatin显著降低了CHF子的RSNA和血北上腺素.
- 西姆瓦斯塔丁治疗使心率的巴罗反射调节正常化,以应对低血压.
结论:
- 类他类药物的非降脂作用包括在CHF中对同情性外流的正常化.
- 西姆瓦斯塔丁改善了实验性心血管衰竭中的自主调节和巴罗反射功能.
- 这些发现表明一种潜在的新治疗策略来管理CHF的进展.
关键词:
非编程性的非编程性.
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