Gendvilene V I, Kudzhmaĭte R A, Iuriavichius I A
Biull Eksp Biol Med. 1988 Jun;105(6):692-4.
In the isolated electrically stimulated right ventricular papillary muscles the onset of hypoxic contracture occurred 7 +/- 1.2 min and reached maximum 29.2 +/- 4.6 min after the onset of hypoxia. Switching off of the stimulation and diltiazem (10(-6) M) or tetrodotoxin (3 X 10(-6) M) administration delayed the development of the hypoxic contracture and decreased its maximum level. The protective action of diltiazem was noted only in the presence of rhythmical stimulation. It was concluded that, in addition to the influx of Ca ions through calcium channels, the influx of Na ions through sodium channels was important in the development of hypoxic contracture.
在分离的电刺激右心室乳头肌中，缺氧性挛缩在缺氧开始后7±1.2分钟出现，并在缺氧开始后29.2±4.6分钟达到最大值。停止刺激并给予地尔硫卓（10⁻⁶ M）或河豚毒素（3×10⁻⁶ M）可延迟缺氧性挛缩的发展并降低其最大程度。地尔硫卓的保护作用仅在有节律性刺激时才被观察到。得出的结论是，除了钙离子通过钙通道内流外，钠离子通过钠通道内流在缺氧性挛缩的发展中也很重要。
