Effects of Ca2+ and epinephrine on Ca2+ recirculation fraction and total Ca2+ handling in canine left ventricles

Effects of Ca2+ and epinephrine on Ca2+ recirculation fraction and total Ca2+ handling in canine left ventricles
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DOI:
10.2170/jjphysiol.48.123
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发表时间:
1998-04-01
期刊:
JAPANESE JOURNAL OF PHYSIOLOGY
影响因子:
--
通讯作者:
Suga, H
Suga, H
中科院分区:
其他
文献类型:
--
作者:
Syuu, Y;Araki, J;Suga, H

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我们研究了冠状动脉内Ca 2+和肾上腺素对离体交叉循环犬心脏制备的左心室(LV)细胞内Ca 2+再循环分数(RF)和总Ca 2+处理的影响。我们分析了在持续心房起搏下偶发性自发性期外收缩后的LV期外收缩后增强(PESP)。所有PESP交替衰减,没有单调衰减。我们从交替PESP中提取指数衰减成分,测定其搏动常数(tau(e)),并计算RF = exp(-1/tau(e))。增加冠状动脉内Ca 2+可略微增加tau(e)和RF,但肾上腺素不改变它们,尽管两种药物均使LV收缩性增强2-3倍。Ca 2+和肾上腺素都不影响交替PESP的正弦衰减。这些结果表明,Ca 2+稍微增强了通过肌浆网的RF,但肾上腺素却没有增强。我们将这些RF数据与LV Ca 2+处理O-2消耗数据相结合,并获得40-110 μ mol/kg作为对照和增强收缩状态下一个心动周期内处理的Ca 2+总量。这些结果表明,这种新的左心室水平的方法似乎更好地理解的Ca 2+质量动力学负责增强肌力干预的机械能。
We investigated the effects of intracoronary Ca2+ and epinephrine on the intracellular Ca2+ recirculation fraction (RF) and total Ca2+ handling in the left ventricle (LV) of the excised cross-circulated canine heart preparation. We analyzed LV postextrasystolic potentiation (PESP) following a spontaneous extrasystole that occurred sporadically under constant atrial pacing. All PESPs decayed in alternans and none decayed monotonically. We extracted an exponential decay component from the alternans PESP, determined its beat constant (tau(e)), and calculated RF = exp(-1/tau(e)), Increased intracoronary Ca2+ slightly increased tau(e) and RF, but epinephrine did not change them, although both agents enhanced LV contractility 2-3 times. Neither Ca2+ nor epinephrine affected the sinusoidal decay of the alternans PESP, These results indicate that RF via the sarcoplasmic reticulum was slightly augmented by Ca2+, but not by epinephrine. We combined these RF data with LV Ca2+ handling O-2 consumption data and obtained 40-110 mu mol/kg as the total amount of Ca2+ handled in one cardiac cycle in the control and enhanced contractile states. These results indicate that this new LV-level approach seems to better the understanding of the Ca2+ mass dynamics responsible for the mechanoenergetics enhanced by inotropic interventions.