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atractyloside/hypoxia
Link salvestatakse lõikelauale
Leht 1 alates 33 tulemused
Isoflurane postconditioning improved long-term neurological outcome possibly via inhibiting the mitochondrial permeability transition pore in neonatal rats after brain hypoxia-ischemia.
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BACKGROUND
Isoflurane postconditioning induces neuroprotection in neonatal rats after hypoxia/ischemia (HI). Here, we evaluated the possible role of inhibiting the mitochondrial permeability transition pore (mPTP) in isoflurane postconditioning-improved long-term neurological outcome after brain
Anoxia-mediated calcium release through the mitochondrial permeability transition pore silences NMDA receptor currents in turtle neurons.
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Mammalian neurons are anoxia sensitive and rapidly undergo excitotoxic cell death when deprived of oxygen, mediated largely by Ca(2+) entry through over-activation of N-methyl-d-aspartate receptors (NMDARs). This does not occur in neurons of the anoxia-tolerant western painted turtle, where a
Extracellular Cl--free-induced cardioprotection against hypoxia/reoxygenation is associated with attenuation of mitochondrial permeability transition pore.
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The isotonic substitution of extracellular chloride by gluconate (extracellular Cl--free) has been demonstrated to elicit cardioprotection by attenuating ischaemia/reperfusion-induced elevation of intracellular chloride ion concentration ([Cl-]i). However, the downstream mechanism underlying the
Efficacy and mechanism of hypoxic postconditioning in salvage of ex vivo human rectus abdominis muscle from hypoxia/reoxygenation injury.
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In reconstructive surgery, skeletal muscle may endure protracted ischemia before reperfusion, which can lead to significant ischemia/reperfusion injury. Ischemic postconditioning induced by brief cycles of reperfusion/reocclusion at the end of ischemia has been shown to salvage skeletal muscle from
[Characteristics of adenine nucleotide translocator in mitochondria of rat cerebral cortex during hypobaric hypoxia exposure].
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The purpose of the present study was to explore the effects of hypoxic exposure on mitochondrial adenine nucleotide translocator (ANT) activity and its characteristics. Male Wistar rats were exposed to hypoxia in a hypobaric chamber simulating high altitude at 5 000 m for 1, 5, 15 and 30 d. Control
Extrarenal and direct renal actions of atractyloside contribute to its acute nephrotoxicity in pentobarbital-anesthetized dogs.
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Acute extrarenal and renal changes were noted following the intravenous administration of atractyloside (ATR) (12.97 and 32.40 mumol/kg) to spontaneously-respiring, pentobarbital-anesthetized dogs. Severe hypoglycemia, respiratory depression and hypoxemia developed within 2 h. These extrarenal
Mitochondrial transmembrane potential and pH gradient during anoxia.
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The effect of anoxia on the mitochondrial transmembrane potential and pH gradient was studied in a preparation of isolated hepatocytes. Transmembrane potential (delta psi) was calculated from the distribution of triphenylmethylphosphonium between the mitochondrial, cytosolic, and extracellular
Role of protein kinase C, PI3 kinase, tyrosine kinases, NO-synthase, KATP channels and MPT pore in the signaling pathway of the cardioprotective effect of chronic continuous hypoxia.
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It was established that adaptation to chronic continuous normobaric hypoxia (CCNH) increases cardiac tolerance to ischemia and reperfusion. It was performed coronary artery occlusion (20 min) and reperfusion (3 h) in Wistar rats. CCNH promoted a decrease in the infarct size/area at risk ratio in
New soft alkylating agents with enhanced cytotoxicity against cancer cells resistant to chemotherapeutics and hypoxia.
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Chloroethylureas (CEU) are soft alkylating agents that covalently bind to beta-tubulin (betaTAC) and affect microtubule polymerization dynamics. Herein, we report the identification of a CEU subset and its corresponding oxazolines, which induce cell growth inhibition, apoptosis, and microtubule
Combination of hypoxic preconditioning and postconditioning does not induce additive protection of ex vivo human skeletal muscle from hypoxia/reoxygenation injury.
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We previously demonstrated that hypoxic preconditioning (HPreC) or postconditioning (HPostC) protected ex vivo human skeletal muscle from hypoxia/reoxygenation injury. Here, we investigated if combined HPreC and HPostC could convey additive protection. Human rectus abdominis muscle strips were
K(ATP) channels and MPTP are involved in the cardioprotection bestowed by chronic intermittent hypobaric hypoxia in the developing rat.
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The aim of this study was to explore the mechanism underlying the cardioprotection bestowed by chronic intermittent hypobaric hypoxia (CIHH) against ischemia/reperfusion (I/R) injury in developing rats. Neonatal male rats were subjected to CIHH treatments that simulated an altitude of 3000 m a.s.l.
Intermittent high altitude hypoxia inhibits opening of mitochondrial permeability transition pores against reperfusion injury.
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The role of mitochondrial permeability transition pore (MPTP) in the mechanism of intermittent high altitude (IHA) hypoxic adaptation is not understood. Therefore, we study whether the protective effect of IHA hypoxia against ischemia-reperfusion injury is accompanied by inhibition of MPTP opening.
Sevoflurane postconditioning improves long-term learning and memory of neonatal hypoxia-ischemia brain damage rats via the PI3K/Akt-mPTP pathway.
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BACKGROUND
Volatile anesthetic postconditioning has been documented to provide neuroprotection in adult animals. Our aim was to investigate whether sevoflurane postconditioning improves long-term learning and memory of neonatal hypoxia-ischemia brain damage (HIBD) rats, and whether the PI3K/Akt
Cyclosporin and carnitine prevent the anoxic death of cultured hepatocytes by inhibiting the mitochondrial permeability transition.
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Cyclosporin A (CyA) and L-carnitine (LC) prevented the killing of cultured hepatocytes by anoxia and rotenone but not by cyanide. Neither CyA nor LC affected the rate or extent of the loss of the mitochondrial membrane potential or the rate or extent of the depletion of ATP. Atractyloside blocked
Calcium preconditioning inhibits mitochondrial permeability transition and apoptosis.
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We tested the hypothesis whether calcium preconditioning (CPC) reduces reoxygenation injury by inhibiting mitochondrial permeability transition (MPT). Cultured myocytes were preconditioned by a brief exposure to 1.5 mM calcium (CPC) and subjected to 3 h of anoxia followed by 2 h of reoxygenation
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