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和EMD-53998对隔离犬心中的氧气消耗的影响

P P de Tombe¹, D Burkhoff, W C Hunter

¹Department of Biomedical Engineering, Johns Hopkins University, School of Medicine, Baltimore, Md. 21205.

|December 1, 1992

概括

这项研究研究了一种敏感剂EMD-53998,研究其对心脏收缩性和心肌效率的影响. 结果显示EMD-53998增加了收缩性,但与现有药物相比没有提供能量优势.

科学领域:

心脏病学心脏病学
药理学药理学是指药理学的学科.

背景情况:

积极的内类药物通常通过提高细胞内 (Ca2+) 来增加心脏收缩性,这可能会由于增加氧气消耗而降低心肌效率.
建议EMD-53998增强收缩蛋白的Ca2+敏感性,可能在不改变Ca2+短暂性的情况下改善收缩性.

研究的目的:

测试EMD-53998增加心脏收缩率而不会降低心肌效率的假设.

主要方法:

心肌氧消耗量 (MVO2) 被测量在隔离的,血液透的狗心脏中,其节奏为每分钟120次.
用化 (CaCl2) 或EMD-53998输注来调节心脏收缩率.

主要成果:

对于CaCl2和EMD-53998.8,MVO2与收缩性有线关系.
在CaCl2和EMD-53998.8之间,在收缩性-MVO2关系中没有观察到显著的差异.

结论:

在狗心中,EMD-53998作为一种强有力的正义内类药物.
与当前的阳性无otropic 药物相比,EMD-53998 没有提供能量优势.

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