Stern M D, Chien A M, Capogrossi M C, Pelto D J, Lakatta E G
Circ Res. 1985 Jun;56(6):899-903. doi: 10.1161/01.res.56.6.899.
By phase contrast microscopy with video length tracking, we followed the sequence of morphological changes in individual isolated rat ventricular myocytes during anoxia followed by reoxygenation. Cells appeared normal during early anoxia. After a duration of anoxia T1, which varied from 17-47 minutes in different cells, each cell abruptly contracted an average of 33% in length to an inert rectangular form presumed to be a rigor state. Cells which were reoxygenated before the onset of rigor showed normal morphology and an unchanged extent of shortening on field stimulation, compared to control. Cells that were reoxygenated after a time in the rigor state, T2, either partially recovered to a shortened rectangular form capable of stimulated twitches or rounded up rapidly to a disordered hypercontracture form. The distribution of T1 was the same for cells which recovered and which hypercontracted. In contrast, the outcome of reoxygenation depended markedly on T2: all cells that were reoxygenated after less than 10 minutes of rigor recovered function, whereas all cells that spent more than 20 minutes in rigor hypercontracted when reoxygenated. The hypercontracture appears to be the cellular analog of the "oxygen paradox" in whole hearts. Its occurrence is reliably related to duration of rigor state but not to duration of hypoxia, because of marked cellular variability in the time of onset of rigor.
通过相差显微镜和视频长度追踪，我们观察了单个分离的大鼠心室肌细胞在缺氧及随后复氧过程中的形态变化序列。在缺氧早期，细胞看起来正常。在不同细胞中持续时间为17 - 47分钟的缺氧期T1之后，每个细胞突然平均收缩33%的长度，变成一种假定为僵硬状态的惰性矩形形态。在僵硬状态出现之前复氧的细胞，与对照相比，在电场刺激下显示出正常形态且缩短程度不变。在处于僵硬状态一段时间T2之后复氧的细胞，要么部分恢复到能够产生刺激抽搐的缩短矩形形态，要么迅速变圆形成无序的超收缩形态。恢复和超收缩的细胞T1分布相同。相比之下，复氧的结果明显取决于T2：在僵硬状态持续不到10分钟后复氧的所有细胞都恢复了功能，而在僵硬状态持续超过20分钟后复氧的所有细胞在复氧时都出现了超收缩。超收缩似乎是全心脏中“氧悖论”的细胞类似物。由于僵硬状态开始时间存在明显的细胞变异性，其发生与僵硬状态的持续时间可靠相关，而与缺氧持续时间无关。
