Vornovitskiĭ E G, Kobrinskiĭ E M, Gallasch M, Ignat'eva V B, Kukushkin N I
Biull Eksp Biol Med. 1989 Dec;108(12):643-6.
The effects of platelet-activating factor (PAF) on the myocardial cell membrane Ca-current (ICa) and Ca-action potential (Ca-AP) were investigated. In double sucrose-gap voltage-clamped frog atrial trabeculae PAF (2 X 10(-7) M) reduced ICa-amplitude to 40-50%; at the same time the IK-amplitude was increased to the same value. These changes of ICa and IK amplitudes were protected by simultaneous action of PAF and PAF antagonist BN 52021 (4 X 10(-6) M). In the partially depolarized (K+0 = 15-20 mM) of the guinea pig myocardial auricles PAF decreased Ca-AP amplitude and Vmax of its upstroke and shortened the Ca-AP duration (intracellular microelectrodes) like the isometric tension responses. These effects were prevented by PAF antagonist U-66985. Histamine was also able to protect from the PAF-induced changes of Ca-AP and tension responses. Our data demonstrated both by direct and by indirect methods of ICa registration in myocardia membrane that PAF induces reversed blocking of ICa. Because the blocking effects of PAF on frog and guinea pig myocardium are identical, these results imply that the mechanisms of PAF action on cold- and warm-blooded animals are similar in principle. The coupling of ICa and IK changes confirm our earlier supposition that PAF-induced Ca-AP shorting can be explained by IK augmentation.
研究了血小板活化因子（PAF）对心肌细胞膜钙电流（ICa）和钙动作电位（Ca-AP）的影响。在双蔗糖间隙电压钳制的蛙心房小梁中，PAF（2×10⁻⁷M）使ICa幅度降低至40% - 50%；同时IK幅度增加到相同值。ICa和IK幅度的这些变化受到PAF与PAF拮抗剂BN 52021（4×10⁻⁶M）同时作用的保护。在豚鼠心肌心耳部分去极化（K⁺₀ = 15 - 20 mM）时，PAF降低Ca-AP幅度及其上升支的Vmax，并缩短Ca-AP持续时间（细胞内微电极），类似于等长张力反应。这些效应被PAF拮抗剂U - 66985阻止。组胺也能够保护免受PAF诱导的Ca-AP和张力反应变化的影响。我们的数据通过心肌细胞膜ICa记录的直接和间接方法均表明，PAF诱导ICa的反向阻断。由于PAF对蛙和豚鼠心肌的阻断作用相同，这些结果意味着PAF对冷血和温血动物的作用机制在原则上是相似的。ICa和IK变化的耦合证实了我们早期的推测，即PAF诱导的Ca-AP缩短可以通过IK增强来解释。
