Gendvilene V I, Narushevichus E V
Biull Eksp Biol Med. 1981 Apr;91(4):403-4.
A 40-minute perfusion of the frog ventricular strip with a hypoxic Ringer solution brings about a decline in action potential duration by 37 plus or minus 10% whereas the contractility is completely suppressed by that time. The time constant of the contractility exponential decline constitutes 8 plus or minus 2 min. the effect of hypoxia is reversible. Complete blockade of the calcium channels by fenigidin (3.5 x 10(-5) M) irreversibly lowers action potential duration by 62 plus or minus 2%. Contraction is completely suppressed on attaining the given level of action potentials. Hypoxia does not virtually affect action potential after the preliminary blockade of the calcium channels by fenigidin. It is suggested that the hypoxic solution mainly blocks the inward current across the calcium channels without affecting the potassium permeability of the sarcolemma. Meanwhile complete suppression of the contractility under hypoxia cannot be accounted for only by the blockade of the calcium channels.
用缺氧任氏液灌注青蛙心室肌条40分钟，动作电位时程下降37±10%，而此时收缩性被完全抑制。收缩性指数下降的时间常数为8±2分钟。缺氧的影响是可逆的。用粉防己定（3.5×10⁻⁵M）完全阻断钙通道可使动作电位时程不可逆地降低62±2%。当动作电位达到给定水平时，收缩被完全抑制。在用粉防己定预先阻断钙通道后，缺氧对动作电位几乎没有影响。提示缺氧溶液主要阻断跨钙通道的内向电流，而不影响肌膜的钾通透性。同时，缺氧时收缩性的完全抑制不能仅用钙通道的阻断来解释。
