2001
DOI: 10.1159/000056116
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The Na<sup>+</sup>/H<sup>+</sup> Exchanger SM-20220 Attenuates Ischemic Injury in in vitro and in vivo Models

Abstract: The aim of this study is to clarify whether the activation of a Na+/H+ exchanger (NHE) is tightly concerned with neuronal and glial cell injury induced by ischemia using a selective NHE inhibitor, SM-20220 (N-(aminoiminomethyl)-1-methyl-1H-indole-2-carboxamide methanesulfonate). Two hours of hypoxia followed by 24 h of reoxygenation induced lactate dehydrogenase (LDH) release, a marker of cell membrane damage, in cultured neurons and glia derived from rats. SM-20220 significantly reduced … Show more

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Cited by 36 publications
(25 citation statements)
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References 21 publications
(26 reference statements)
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“…9 Surprisingly, inhibition of the NHE has been reported to protect rats from ischemia-induced brain damage. [10][11][12][13] However, these effects may not be due to the block of the NHE-mediated control of intracellular pH, but due to the block of free fatty acid efflux 14 and block of neutrophil accumulation. 10 To study the role of potassium and acidification in neuronal apoptosis, we investigated the role of the outward delayed rectifier potassium current, changes of pH i and the NHE in apoptosis of cerebellar granule neurons.…”
Section: Introductionmentioning
confidence: 99%
“…9 Surprisingly, inhibition of the NHE has been reported to protect rats from ischemia-induced brain damage. [10][11][12][13] However, these effects may not be due to the block of the NHE-mediated control of intracellular pH, but due to the block of free fatty acid efflux 14 and block of neutrophil accumulation. 10 To study the role of potassium and acidification in neuronal apoptosis, we investigated the role of the outward delayed rectifier potassium current, changes of pH i and the NHE in apoptosis of cerebellar granule neurons.…”
Section: Introductionmentioning
confidence: 99%
“…There is a hypothesis that glial swelling and brain edema are caused by the activation of the NHE in cerebral ischemia. 20) In stroke patients, a contributory cause of early death in cortical infarcts is believed to be edema around the ischemic lesion, leading to transtentorial herniation, 21) and this condition is associated with an 80% mortality.…”
Section: Discussionmentioning
confidence: 99%
“…There is a hypothesis that glial swelling and brain edema are caused by the activation of the NHE in cerebral ischemia. 20) In stroke patients, a contributory cause of early death in cortical infarcts is believed to be edema around the ischemic lesion, leading to transtentorial herniation, 21) and this condition is associated with an 80% mortality.22) Therefore, the ability of SM-20220 to reduce edema formation is a very beneficial property for its therapeutic efficacy.The protective effect of SM-20220 was attenuated when administration was started 2 h after occlusion. The therapeutic time window is one of the most important factors in clinical therapy.…”
mentioning
confidence: 99%
“…Activation of NHE-1 has been shown to be a pivotal event in cell damage induced by ischemia and reperfusion in the brain (Horikawa et al, 2001;Hwang et al, 2008;Luo et al, 2005), heart (Liu et al, 1997;Murphy et al, 1991;Wang et al, 2003), liver (Gores et al, 1989), and lungs (Rios et al, 2005). Here we will review recent findings implicating NHE-1 activation as a critical event in the pathogenesis of cellular dysfunction after cerebral ischemia, and the growing evidence supporting the use of NHE inhibitors as neuroprotective agents following cerebral ischemia.…”
mentioning
confidence: 97%