Ito K, Karaki H, Urakawa N
Jpn J Pharmacol. 1979 Jun;29(3):467-76. doi: 10.1254/jjp.29.467.
Effects of palytoxin (PTX) on isolated papillary muscles of guinea pigs were studied in an attempt to elucidate the mechanical and electrical activities. Inotropic effects of PTX above 3 x 10(-9) g/ml; an early positive inotropic effect, slowly developing contracture accompanied by decline in phasic tension, appearance of aftercontractions and arrhythmias at high doses. The positive inotropic effect of PTX was enhanced in high Ca2+ medium but was not modified by propranolol. PTX induced a sustained depolarization and decrease in the amplitude, upstroke velocity and duration of action potential. During development of depolarization, arrhythmias occurred, which lasted for 5--10 min and reappeared 30--60 min after. Oscillatory afterpotential often appeared. Neither reserpine nor practolol prevented the PTX-induced arrhythmia while propranolol prevented it. Tetrodotoxin slowed the development of depolarization due to PTX and inhibited PTX-arrhythmias. In low Na+ medium, PTX exerted fewer effects on resting and action potentials and produced no arrhythmia. The results suggest that PTX-induced depolarization is responsible for the generation of contracture and arrhythmia and that the depolarization is due to the change in membrane Na permeability.
为阐明机械和电活动,研究了海葵毒素(PTX)对豚鼠离体乳头肌的影响。PTX浓度高于3×10⁻⁹ g/ml时具有变力作用;早期出现正性变力作用,随后缓慢发展为挛缩,伴有相位张力下降,高剂量时出现后收缩和心律失常。PTX的正性变力作用在高钙培养基中增强,但不受普萘洛尔影响。PTX诱导持续去极化,并使动作电位的幅度、上升速度和持续时间降低。在去极化过程中出现心律失常,持续5 - 10分钟,30 - 60分钟后再次出现。常出现振荡后电位。利血平和醋氨心安均不能预防PTX诱导的心律失常,而普萘洛尔可以预防。河豚毒素减缓了PTX引起的去极化发展,并抑制了PTX诱导的心律失常。在低钠培养基中,PTX对静息电位和动作电位的影响较小,且不产生心律失常。结果表明,PTX诱导的去极化是挛缩和心律失常产生的原因,且去极化是由于膜钠通透性的改变。