Shimizu J, Araki J, Mizuno J, Lee S, Syuu Y, Hosogi S, Mohri S, Mikane T, Takaki M, Taylor T W, Suga H
Department of Physiology II, Okayama University Medical School, Okayama 700-8558, 634-8521 Japan.
Am J Physiol. 1998 Dec;275(6):H2325-33. doi: 10.1152/ajpheart.1998.275.6.H2325.
Ca2+ handling in excitation-contraction coupling requires considerable O2 consumption (VO2) in cardiac contraction. We have developed an integrative method to quantify total Ca2+ handling in normal hearts. However, its direct application to failing hearts, where futile Ca2+ cycling via the Ca2+-leaky sarcoplasmic reticulum (SR) required an increased Ca2+ handling VO2, was not legitimate. To quantify total Ca2+ handling even in such failing hearts, we combined futile Ca2+ cycling with Ca2+ handling VO2 and the internal Ca2+ recirculation fraction via the SR. We applied this method to the canine heart mechanoenergetics before and after intracoronary ryanodine at nanomolar concentrations. We found that total Ca2+ handling per beat was halved after the ryanodine treatment from approximately 60 micromol/kg left ventricle before ryanodine. We also found that futile Ca2+ cycling via the SR increased to >1 cycle/beat after ryanodine from presumably zero before ryanodine. These results support the applicability of the present method to the failing hearts with futile Ca2+ cycling via the SR.
兴奋-收缩偶联过程中的钙离子处理在心脏收缩时需要消耗大量氧气（VO₂）。我们已经开发出一种综合方法来量化正常心脏中的总钙离子处理情况。然而，将其直接应用于衰竭心脏并不合理，因为通过钙泄漏的肌浆网（SR）进行的无效钙循环会导致钙离子处理所需的VO₂增加。为了量化即使在这种衰竭心脏中的总钙离子处理情况，我们将无效钙循环与钙离子处理VO₂以及通过SR的内部钙再循环分数相结合。我们将此方法应用于冠状动脉内注射纳摩尔浓度的ryanodine前后的犬心脏机械能量学研究。我们发现，ryanodine处理后，每搏总钙离子处理量从ryanodine处理前左心室约60微摩尔/千克减半。我们还发现，通过SR的无效钙循环从ryanodine处理前可能为零增加到ryanodine处理后大于1次/搏。这些结果支持了本方法对通过SR进行无效钙循环的衰竭心脏的适用性。
