Maier L S, Barckhausen P, Weisser J, Aleksic I, Baryalei M, Pieske B
Abteilung Kardiologie und Pneumologie, Zentrum Innere Medizin, Georg-August-Universität Göttingen, 37075 Göttingen, Germany.
Am J Physiol Heart Circ Physiol. 2000 Sep;279(3):H952-8. doi: 10.1152/ajpheart.2000.279.3.H952.
Physiologically, human atrial and ventricular myocardium are coupled by an identical beating rate and rhythm. However, contractile behavior in atrial myocardium may be different from that in ventricular myocardium, and little is known about intracellular Ca(2+) handling in human atrium under physiological conditions. We used rapid cooling contractures (RCCs) to assess sarcoplasmic reticulum (SR) Ca(2+) content and the photoprotein aequorin to assess intracellular Ca(2+) transients in atrial and ventricular muscle strips isolated from nonfailing human hearts. In atrial myocardium (n = 19), isometric twitch force frequency dependently (0. 25-3 Hz) increased by 78 +/- 25% (at 3 Hz; P < 0.05). In parallel, aequorin light signals increased by 111 +/- 57% (P < 0.05) and RCC amplitudes by 49 +/- 13% (P < 0.05). Similar results were obtained in ventricular myocardium (n = 13). SR Ca(2+) uptake (relative to Na(+)/Ca(2+) exchange) frequency dependently increased in atrial and ventricular myocardium (P < 0.05). With increasing rest intervals (1-240 s), atrial myocardium (n = 7) exhibited a parallel decrease in postrest twitch force (at 240 s by 68 +/- 5%, P < 0.05) and RCCs (by 49 +/- 10%, P < 0.05). In contrast, postrest twitch force and RCCs significantly increased in ventricular myocardium (n = 6). We conclude that in human atrial and ventricular myocardium the positive force-frequency relation results from increased SR Ca(2+) turnover. In contrast, rest intervals in atrial myocardium are associated with depressed contractility and intracellular Ca(2+) handling, which may be due to rest-dependent SR Ca(2+) loss (Ca(2+) leak) and subsequent Ca(2+) extrusion via Na(+)/Ca(2+) exchange. Therefore, the influence of rate and rhythm on mechanical performance is not uniform in atrial and ventricular myocardium.
在生理状态下，人类心房和心室心肌通过相同的搏动频率和节律相互耦合。然而，心房心肌的收缩行为可能与心室心肌不同，并且在生理条件下人类心房细胞内钙（Ca(2+)）处理的情况鲜为人知。我们使用快速冷却挛缩（RCCs）来评估肌浆网（SR）的Ca(2+)含量，并使用光蛋白水母发光蛋白来评估从无衰竭人类心脏分离出的心房和心室肌条中的细胞内Ca(2+)瞬变。在心房心肌（n = 19）中，等长收缩力随频率（0.25 - 3 Hz）依赖性增加，在3 Hz时增加了78±25%（P < 0.05）。同时，水母发光蛋白光信号增加了111±57%（P < 0.05），RCC幅度增加了49±13%（P < 0.05）。在心室心肌（n = 13）中也获得了类似结果。心房和心室心肌中SR Ca(2+)摄取（相对于Na(+)/Ca(2+)交换）随频率依赖性增加（P < 0.05）。随着静息间隔时间增加（1 - 240秒），心房心肌（n = 7）静息后收缩力（在240秒时下降68±5%，P < 0.05）和RCCs（下降49±10%，P < 0.05）呈平行下降。相反，心室心肌（n = 6）静息后收缩力和RCCs显著增加。我们得出结论，在人类心房和心室心肌中，正向力 - 频率关系源于SR Ca(2+)周转率增加。相比之下，心房心肌中的静息间隔与收缩力降低和细胞内Ca(2+)处理有关，这可能是由于依赖静息的SR Ca(2+)丢失（Ca(2+)泄漏）以及随后通过Na(+)/Ca(2+)交换进行的Ca(2+)外排。因此，频率和节律对机械性能的影响在心房和心室心肌中并不一致。
