Roulet M J, Coburn R F
Circ Res. 1981 Oct;49(4):997-1002. doi: 10.1161/01.res.49.4.997.
We investigated the mechanism of oxygen-induced contractions in ductus arteriosus isolated from neonatal guinea pig. A preparation equilibrated at low Po2 (less than 40 mm Hg) displayed a steady membrane potential of -54.8 mV. Application of oxygen (Po2 (less than approximately or equal to 300 mm Hg) resulted in: (1) stepwise development of tension coupled to action potentials and (2) sustained membrane depolarization to -32.9 mV associated with tonic contraction. Mechanical sensitivity to oxygen persisted at any[K]o up to 126 mM, and tension was always larger at a given [K]o or a given membrane potential with high Po2 than with low Po2. The change in membrane potential per decade change in [K]o was 35 mV at low Po2 and 16 mV at high Po2. Oxygen contractions occurred when the ductal strips were bathed in K-free media or exposed to ouabain. We conclude that oxygen caused a conductance change in the sarcolemma resulting in depolarization, which is coupled to contraction. There is also evidence of a membrane potential-independent contraction mechanism.
我们研究了从新生豚鼠分离的动脉导管中氧诱导收缩的机制。在低氧分压（小于40 mmHg）下平衡的标本显示出稳定的膜电位为 -54.8 mV。施加氧气（氧分压小于或约等于300 mmHg）导致：（1）与动作电位相关的张力逐步发展，以及（2）与强直性收缩相关的膜持续去极化至 -32.9 mV。在高达126 mM的任何细胞外钾浓度下，对氧的机械敏感性持续存在，并且在给定的细胞外钾浓度或给定的膜电位下，高氧分压时的张力总是比低氧分压时更大。在低氧分压下，细胞外钾浓度每变化十倍，膜电位变化为35 mV；在高氧分压下为16 mV。当动脉导管条浸泡在无钾培养基中或暴露于哇巴因时，会出现氧收缩。我们得出结论，氧导致肌膜电导变化，从而引起去极化，这与收缩相关。也有证据表明存在一种与膜电位无关的收缩机制。
