Zijlstra F J, Vincent J E
Gen Pharmacol. 1986;17(5):585-8. doi: 10.1016/0306-3623(86)90099-6.
The leukotriene C4 (LTC4)-induced contraction and thromboxane A2 (TxA2) release of the guinea pig lung parenchymal (GPLP) strip are both inhibited by the beta 2-adrenergic agent salbutamol. The effect of LTC4 is restored to nearly normal by the beta-adrenergic antagonist sotalol. The latter substance alone also induces a contraction in the GPLP strip and potentiates the contractions and the TxA2 release of LTC4. During the sotalol-induced contractions, no TxA2 release occurs. An antihistaminic, mepyramine had no effect on the sotalol-induced contraction. When sotalol is added repeatedly to a GPLP strip, only the first time a contraction occurs.
白三烯C4(LTC4)诱导的豚鼠肺实质(GPLP)条收缩及血栓素A2(TxA2)释放均受到β2肾上腺素能药物沙丁胺醇的抑制。β肾上腺素能拮抗剂索他洛尔可使LTC4的作用恢复至接近正常水平。单独使用后一种物质也可诱导GPLP条收缩,并增强LTC4的收缩作用及TxA2释放。在索他洛尔诱导的收缩过程中,未出现TxA2释放。抗组胺药美吡拉敏对索他洛尔诱导的收缩无影响。当向GPLP条反复添加索他洛尔时,仅首次添加时会出现收缩。