Kasamaki Y, Guo A C, McDonald T F
Department of Physiology and Biophysics, Dalhousie University, Halifax, NS, Canada.
Cardiovasc Res. 1997 May;34(2):313-22. doi: 10.1016/s0008-6363(97)00021-7.
Developed tension in guinea-pig papillary muscles is depressed by prolonged hypoxia; subsequent reoxygenation leads to a partial recovery that stabilizes after an early period of arrhythmia. We have investigated whether hypoxic preconditioning in these muscles (1) improves the recovery of developed tension, (2) protects against arrhythmia, and (3) causes other significant electromechanical changes.
Papillary muscles stimulated at 1 Hz were superfused with oxygenated Krebs solution for 60 min and either preconditioned (5 min of 3 Hz pacing substrate-free hypoxic conditions, 10 min of normoxic recovery) or equilibrated for an extra 15 min. Muscles were subsequently challenged with substrate-free hypoxia (1 Hz), and reoxygenated (1 Hz) for 60 min. Contractile performance, action potential parameters, and indicators of arrhythmic activity were measured in 10 preconditioned and 10 non-preconditioned muscles.
Developed tension in preconditioned muscles declined to the same level (10-15% control) as in non-preconditioned muscles after 60 min hypoxia. A notable difference was that developed tension in the preconditioned muscles failed to rebound during mid-hypoxia, a hallmark feature in non-preconditioned muscles. The action potential duration and overshoot collapsed at a significantly faster rate in hypoxic preconditioned muscles. Action potential recovery during reoxygenation was similar in the two groups of muscles, but recovery of developed tension was significantly stronger in preconditioned (76.7 +/- 5.4%) than in non-preconditioned (42.9 +/- 1.7%) muscles (P < 0.001). Reoxygenation provoked arrhythmic activity in all muscles, but the summed average duration was shorter (5.5 +/- 1.0 vs. 9.4 +/- 1.5 min) (P < 0.05) in the preconditioned muscles.
Hypoxic preconditioning can significantly enhance post-hypoxia recovery of developed tension, and significantly attenuate arrhythmic activity, in guinea-pig papillary muscles.
长时间缺氧会使豚鼠乳头肌产生的张力降低；随后再给氧会导致部分恢复，在早期心律失常期后恢复稳定。我们研究了这些肌肉中的缺氧预处理是否（1）改善产生张力的恢复情况，（2）预防心律失常，以及（3）引起其他显著的机电变化。
以1Hz频率刺激的乳头肌用含氧的 Krebs 溶液灌注60分钟，要么进行预处理（在无底物的缺氧条件下以3Hz起搏5分钟，常氧恢复10分钟），要么再平衡15分钟。随后肌肉接受无底物缺氧（1Hz）刺激，并再给氧（1Hz）60分钟。在10块预处理肌肉和10块未预处理肌肉中测量收缩性能、动作电位参数和心律失常活动指标。
缺氧60分钟后，预处理肌肉产生的张力下降到与未预处理肌肉相同的水平（对照的10 - 15%）。一个显著的差异是，预处理肌肉产生的张力在缺氧中期没有出现未预处理肌肉的标志性特征——反弹。缺氧预处理肌肉的动作电位持续时间和超射以显著更快的速度消失。两组肌肉在再给氧期间动作电位的恢复情况相似，但预处理肌肉（76.7±5.4%）产生张力的恢复明显强于未预处理肌肉（42.9±1.7%）（P<0.001）。再给氧在所有肌肉中都引发了心律失常活动，但预处理肌肉的总平均持续时间较短（5.5±1.0对9.4±1.5分钟）（P<0.05）。
缺氧预处理可显著增强豚鼠乳头肌缺氧后产生张力的恢复，并显著减轻心律失常活动。
