在缺氧收缩功能障碍中,Ca2(+) 依存和Ca2(+) 独立机制的相对作用
1Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205.
Circulation
|August 1, 1990
概括
缺氧性心力衰竭不是由低水平引起的. 相反,无机酸盐 (Pi) 的积累,以及在较小程度上,酸性,会在缺氧期间损害心肌收缩.
科学领域:
- 心血管生理学心血管生理学
- 代谢调节 代谢调节 代谢调节
- 心脏动力学心脏动力学
背景情况:
- 心脏收缩功能障碍是低氧和代谢抑制的已知后果.
- 确切的机制,无论是由于减少激活剂或积累抑制代谢物,仍在争论中.
研究的目的:
- 区分细胞内 ([Ca2+]i) 和无机 ([Pi]) 在缺氧收缩功能障碍中的作用.
- 为了研究细胞内pH值 (pHi) 在缺氧期间对心脏功能的影响.
主要方法:
- 使用过的充血心经经受控低氧条件 (10% O2) 条件.
- 采用核磁共振 (NMR) 光谱,包括-19 NMR,以测量[Ca2+]i,[Pi]和pHi.
- 量化左心室发达压力 (LVDP) 来评估收缩功能.
主要成果:
- 缺氧使LVDP降低到对照值的60%左右.
- 在缺氧期间,NMR显示增加了[Pi]和轻微的细胞内酸化 (降低pHi).
- 增加的[Pi]和减少的pHi都与减少的LVDP相关,其中[Pi]具有主导影响.
- 透气结束时的[Ca2+]i没有变化,而最大抽缩[Ca2+]i矛盾地增加;Ca2+短暂幅度与压力下降无关.
结论:
- 轻度稳定状态低氧的收缩性衰竭主要由无机酸盐 ([Pi]) 的积累介导.
- 细胞内酸性 (H+积累) 也有助于,但是次要的, [Pi] 导致缺氧功能障碍.
- 在这些条件下,活性剂 ([Ca2+]i) 的可用性或调节性降低并不是收缩障碍的主要原因.
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