Tenner T E, McNeill J H, Carrier O
Eur J Pharmacol. 1978 Aug 15;50(4):359-67. doi: 10.1016/0014-2999(78)90141-3.
Experiments using electrically stimulated rabbit left atria have demonstrated that supersensitivity to the inotropic effects of norepinephrine can be induced by either chronic reserpine pretreatment or hypothermia (lowering the temperature of the bathing medium). These two experimental conditions for inducing supersensitivity were not additive implying that they shared a common mechanism of action. Norepinephrine had no significant effect on the amplitude of a potentiated contraction of the rabbit atrium when the temperature was reduced from 37 to 30 degrees C or following pretreatment with reserpine (30 or 37 degrees C). Under these same conditions the ED50 of norepinephrine on the normal contraction was reduced. It is concluded that both reserpine pretreatment and hypothermia induce supersensitivity to the inotropic effects of norepinephrine by enhancing the cellular store of activator calcium while not affecting the ability of norepinephrine to release activator calcium.
使用电刺激兔左心房的实验表明,慢性利血平预处理或低温(降低浴液温度)均可诱导对去甲肾上腺素变力作用的超敏反应。这两种诱导超敏反应的实验条件并无叠加效应,这意味着它们具有共同的作用机制。当温度从37℃降至30℃或经利血平预处理后(30℃或37℃),去甲肾上腺素对兔心房增强收缩的幅度无显著影响。在相同条件下,去甲肾上腺素对正常收缩的半数有效量降低。结论是,利血平预处理和低温均通过增加细胞内激活钙的储存而不影响去甲肾上腺素释放激活钙的能力,从而诱导对去甲肾上腺素变力作用的超敏反应。