R 56865

Known as: R-56865, R56865 
 
National Institutes of Health

Papers overview

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2008
2008
Reactive oxygen species (ROS) and intracellular Ca(2+) overload play key roles in myocardial ischemia-reperfusion (IR) injury but… (More)
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2000
2000
1. Persistent sodium channel activity was recorded before and during hypoxia from cell-attached and inside-out patches obtained… (More)
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1999
1999
The effects of bepridil, a potent antiarrhythmic drug, on the activity of ATP-sensitive K(+) (K(ATP)) channels and Na… (More)
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1996
1996
 The inhibitors of the Na+/H+-exchange (NHE1) system Hoe 694 and Hoe 642 possess cardioprotective effects in ischaemia… (More)
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1995
1995
Anoxic depolarization (AD) and failure of ion homeostasis play an important role in ischemia-induced neuronal injury. In the… (More)
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1995
1995
We present in this report the characteristics of the damage induced by 6-hydroxydopamine and H2O2 on bovine chromaffin cells in… (More)
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1995
1995
This study was carried out to define the effects of various Ca2+ channel modulatory drugs on mitochondrial Ca2+ movements. Bovine… (More)
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1995
1995
We investigated the antiischemic and antiarrhythmic effects of R 56865 in pentobarbital-anesthetized, open-chest rabbits… (More)
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1992
1992
The Na+/Ca2+ overload inhibitor R 56865 (N-[1-[4-(4-fluorophenoxy)-butyl]-4-piperidinyl)-N-methyl-2- benzothiazolamine) has been… (More)
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1991
1991
Intracellular Ca2+ overload is considered to be the final pathway leading to cell death under pathological conditions. However… (More)
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