Early reperfusion levels of Na(+) and Ca(2+) are strongly associated with postischemic functional recovery but are disassociated from K(ATP) channel-induced cardioprotection.
Early reperfusion levels of Na(+) and Ca(2+) are strongly associated with postischemic functional recovery but are disassociated from K(ATP) channel-induced cardioprotection.
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Na()和Ca(2)的早期再灌注水平与缺血后功能恢复密切相关，但与K(ATP)通道诱导的心脏保护无关。
DOI：
10.1016/j.yjmcc.2004.05.010
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发表时间：
2004
期刊：
影响因子：
--
通讯作者：
Pike,MartinM
中科院分区：
文献类型：
--
作者：
Takayama,Eiichi;Guo,Ling-Ling;Digerness,StanleyB;Pike,MartinM
我们之前证明，吡那地尔不会影响心肌缺血期间的 Na (+)(i) 积累、细胞能量消耗或酸中毒，但会显着改善再灌注期间的阳离子/能量状态。我们研究了后一种效应在 K (ATP) 通道诱导的心脏保护中的作用。对灌注的大鼠心脏采用 (23) Na 和 (31) P 核磁共振波谱，通过短暂输注哇巴因和/或 RbCl 来改变再灌注 Na (+)(i)，以暂时降低或增加 Na (+)/K (+) ATP 酶活性。吡那地尔或哇巴因各自的功能恢复（% LVDP-R）的增加和减少在很大程度上不因彼此的存在而改变。哇巴因极大地改变了早期再灌注Na (+)(i) 和细胞能量，并且与% LVDP-R 呈线性关系。吡那地尔将这些关系转变为更高％的 LVDP-R。增加早期再灌注Na (+)(i) 会降低% LVDP-R，但不会减弱吡那地尔改善% LVDP-R 的能力。吡那地尔诱导的 LVDP-R 百分比改善中，大约 75% 和 45% 可能分别与早期再灌注 Na (+)(i) 和细胞能量无关。吡那地尔和 RbCl 输注均减弱哇巴因再灌注 Na (+)(i) 的升高，但 RbCl 并未改善 % LVDP-R。原子吸收组织Ca (2+) 测量表明，吡那地尔减少了晚期再灌注Ca (2+) 摄取，但没有减少早期再灌注Ca (2+)，其有益作用是抵抗哇巴因诱导的早期再灌注Ca (2+) 增加。总之，K (ATP) 通道诱导的心脏保护不需要在缺血期间调节 Na (+)(i) 积累、细胞能量消耗或酸中毒。 K (ATP) 通道诱导的心脏保护在很大程度上独立于其诱导的加速再灌注 Na (+)(i) 恢复，并且不需要组织 Ca (2+) 的早期再灌注减少。不能排除早期再灌注细胞能量的更大作用。
We previously demonstrated that pinacidil does not affect Na (+)(i) accumulation, cellular energy depletion, or acidosis during myocardial ischemia, but dramatically improves the cationic/energetic status during reperfusion. We investigated the role of this latter effect in K (ATP) channel-induced cardioprotection. Employing (23) Na and (31) P nuclear magnetic resonance spectroscopy with perfused rat hearts, reperfusion Na (+)(i) was altered with brief infusions of ouabain and/or RbCl to transiently decrease or increase Na (+)/K (+) ATPase activity. The increases and decreases in functional recovery (% LVDP-R) with pinacidil or ouabain, respectively, were largely unaltered by each other's presence. Early reperfusion Na (+)(i) and cellular energy were greatly altered by ouabain and indicated linear relationships with% LVDP-R. Pinacidil shifted these relationships to higher% LVDP-R. Increasing early reperfusion Na (+)(i) decreased% LVDP-R but did not diminish pinacidil's capacity to improve% LVDP-R. Approximately 75% and 45% of the pinacidil-induced improvements in% LVDP-R, could be disassociated from early reperfusion Na (+)(i) and cellular energy, respectively. Both pinacidil and RbCl infusion blunted ouabain's elevation of reperfusion Na (+)(i), but RbCl did not improve% LVDP-R. Atomic absorption tissue Ca (2+) measurements indicated that pinacidil reduced late reperfusion Ca (2+) uptake, but did not reduce early reperfusion Ca (2+), and its beneficial effects were resistant to ouabain-induced early reperfusion Ca (2+) increases. In conclusion, K (ATP) channel-induced cardioprotection does not require moderation of Na (+)(i) accumulation, cellular energy depletion, or acidosis during ischemia. K (ATP) channel-induced cardioprotection is largely independent of the accelerated reperfusion Na (+)(i) recovery it induces and does not require early reperfusion reductions of tissue Ca (2+). A larger role for early reperfusion cellular energy cannot be excluded.
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影响因子：
20.1
作者：
Imahashi, K;Nishimura, T;Kusuoka, H
通讯作者：
Kusuoka, H
影响因子：
20.1
作者：
Sato, T;O'Rourke, B;Marbán, E
通讯作者：
Marbán, E
影响因子：
37.8
作者：
Gumina, RJ;Buerger, E;Gross, GJ
通讯作者：
Gross, GJ
影响因子：
5
作者：
WOLLEBEN, CD;SANGUINETTI, MC;SIEGL, PKS
通讯作者：
SIEGL, PKS
Na 积累会增加 Ca2+ 超载并损害缺氧大鼠心脏的功能。
影响因子：
5
作者：
Tani,M;Neely,JR
通讯作者：
Neely,JR