Effects of MgATP on ATP utilization and force under normal and simulated ischaemic conditions in rat cardiac trabeculae

Effects of MgATP on ATP utilization and force under normal and simulated ischaemic conditions in rat cardiac trabeculae
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DOI:
10.1007/s004240100667
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发表时间:
2001-10-01
影响因子:
4.5
通讯作者:
Stienen, GJM
Stienen, GJM
中科院分区:
医学3区
文献类型:
--
作者:
Ebus, JP;Papp, Z;Stienen, GJM

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在正常(pH 7.0)和模拟缺血(pH 6.2,30 mM添加的P-i)条件下,在20 +/-1 ℃下,在去皮大鼠小梁中研究了ATP利用率和等长力对[MgATP]的依赖性。在饱和[Ca 2 +]时,5 mM MgATP(A(0))的平均(+/- SEM)ATP利用率为0.48 +/-0.03 mM/s,力(F-0)为37 +/-2 kN/m(2)。在正常条件下,10 μ M MgATP时,ATP利用率逐渐下降至A(0)的66 +/-3%,而力增加至F-0的169 +/-7%。在缺血条件下,10 μ M MgATP时,ATP利用率从A(0)的30 +/-5%降至11 +/-2%,而力从F-0的12 +/-4%增至97 +/-7%,增加了8倍。在缺血条件下,半数最大ATP利用率(Km)时的[MgATP]为21 +/-3 μ M。在pH 7.0时,K-m估计小于10 μ M。这些结果表明,随着MgATP的减少,张力成本显著降低。在缺血条件下,观察到力和ATP利用的Ca 2+敏感性的平行变化,对应于1.3 pCa单位。将[MgATP]从0.5 mM降低至0.05 mM导致了Ca 2+敏感性的这种变化的适度逆转。这些变化的Ca 2+敏感性是一致的,在缺血期间的主动力量和力相关的ATP利用率显着减少,但不足以解释缺血性挛缩,主动力量的发展的基础上。
The dependency of ATP utilization and isometric force on [MgATP] was studied in skinned rat trabeculae under normal (pH 7.0) and simulated ischaemic (pH 6.2, 30 mM added P-i) conditions at 20 +/-1 degreesC. At saturating [Ca2+], mean (+/- SEM) ATP utilization at 5 mM MgATP (A(0)) was 0.48 +/-0.03 mM/s and force (F-0) was 37 +/-2 kN/m(2). At 10 muM MgATP under normal conditions ATP utilization decreased gradually to 66 +/-3% of A(0), and force increased to 169 +/-7% of F-0, Under ischaemic conditions at, 10 muM MgATP, ATP utilization decreased from 30 +/-5% to 11 +/-2% of A(0) whereas force increased eight-fold from 12 +/-4% to 97 +/-7% of F-0. The [MgATP] at half-maximal ATP utilization (K-m) under ischaemic conditions was 21 +/-3 muM. At pH 7.0, K-m was estimated to be less than 10 muM. These results show that tension cost decreases markedly with decreasing MgATP. Under ischaemic conditions parallel changes in Ca2+ sensitivity of force and ATP utilization were observed, corresponding to 1.3 pCa units. Reducing [MgATP] from 0.5 to 0.05 mM caused a modest reversal of this change in Ca2+ sensitivity. These changes in Ca2+ sensitivity are consistent with a marked reduction in active force and force-related ATP utilization during ischaemia but are insufficient to explain the ischaemic contracture, on the basis of active force development.