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• W2156989131 abstract "Na⁺/H⁺ exchanger isoform 1 (NHE1) is a major acid extrusion mechanism after intracellular acidosis. We hypothesized that stimulation of NHE1 after cerebral ischemia contributes to the disruption of Na⁺ homeostasis and neuronal death. In the present study, expression of NHE1 was detected in cultured mouse cortical neurons. Three hours of oxygen and glucose deprivation (OGD) followed by 21 h of reoxygenation (REOX) led to 68 ± 10% cell death. Inhibition of NHE1 with the potent inhibitor cariporide (HOE 642) or genetic ablation of NHE1 reduced OGD-induced cell death by ∼40–50% (<i>p</i> < 0.05). In NHE1^+/+ neurons, OGD caused a twofold increase in [Na⁺]_i, and 60 min REOX triggered a sevenfold increase. Genetic ablation of NHE1 or HOE 642 treatment had no effects on the OGD-mediated initial Na⁺_i rise but reduced the second phase of Na⁺_i rise by ∼40–50%. In addition, 60 min REOX evoked a 1.5-fold increase in [Ca²⁺]_i in NHE1^+/+ neurons, which was abolished by inhibition of either NHE1 or reverse-mode operation of Na⁺/Ca²⁺ exchange. OGD/REOX-mediated mitochondrial Ca²⁺ accumulation and cytochrome <i>c</i> release were attenuated by inhibition of NHE1 activity. In an <i>in vivo</i> focal ischemic model, 2 h of left middle cerebral artery occlusion followed by 24 h of reperfusion induced 84.8 ± 8.0 mm³ infarction in NHE1^+/+ mice. NHE1^+/+ mice treated with HOE 642 or NHE1 heterozygous mice exhibited a ∼33% decrease in infarct size (<i>p</i> < 0.05). These results imply that NHE1 activity disrupts Na⁺ and Ca²⁺ homeostasis and contributes to ischemic neuronal damage." @default.
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• W2156989131 modified "2023-10-18" @default.
• W2156989131 title "Measurement of patient perceptions of pain and disability in relation to total hip replacement: the place of the Oxford hip score in mixed methods" @default.
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• W2156989131 doi "https://doi.org/10.1136/qshc.8.4.228" @default.
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