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Sivu 1 alkaen 78 tuloksia
Desflurane-induced post-conditioning against myocardial infarction is mediated by calcium-activated potassium channels: role of the mitochondrial permeability transition pore.
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BACKGROUND
Desflurane (DES)-induced preconditioning is mediated by large-conductance calcium-activated potassium channels (BK(Ca)). Whether BK(Ca) are involved in anaesthetic-induced post-conditioning is unknown. We tested the hypothesis that DES-induced post-conditioning is mediated by BK(Ca)
Nitric oxide donors protect murine myocardium against infarction via modulation of mitochondrial permeability transition.
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Mitochondrial permeability transition (MPT) pores have recently been implicated as a potential mediator of myocardial ischemic injury. Nitric oxide (NO) donors induce a powerful late phase of cardioprotection against ischemia-reperfusion injury; however, the cellular mechanisms involved are poorly
Role of the mitochondrial permeability transition pore in TNF-alpha-induced recovery of ventricular contraction and reduction of infarct size in isolated rat hearts subjected to ischemia/reperfusion.
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Pretreatment with tumor necrosis factor-alpha (TNF-alpha) is known to trigger cardioprotection. TNF-alpha can activate multiple downstream signaling cascades. However, it is not known whether the mitochondrial permeability transition pore (MitoPTP) is involved in TNF-alpha-induced cardioprotection.
Inhibition of glycogen synthase kinase enhances isoflurane-induced protection against myocardial infarction during early reperfusion in vivo.
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Inhibition of glycogen synthase kinase (GSK)-beta protects against ischemia-reperfusion injury. Brief exposure to isoflurane before and during early reperfusion after coronary artery occlusion also protects against infarction. Whether GSK-beta mediates this action is unknown. We tested the
Roles of endothelial nitric oxide synthase (eNOS) and mitochondrial permeability transition pore (MPTP) in epoxyeicosatrienoic acid (EET)-induced cardioprotection against infarction in intact rat hearts.
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We previously demonstrated that 11,12 and 14,15-epoxeicosatrienoic acids (EETs) produce cardioprotection against ischemia-reperfusion injury in dogs and rats. Several signaling mechanisms have been implicated in the cardioprotective actions of the EETs; however, their mechanisms remain largely
Noble gases without anesthetic properties protect myocardium against infarction by activating prosurvival signaling kinases and inhibiting mitochondrial permeability transition in vivo.
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BACKGROUND
The anesthetic noble gas, xenon, produces cardioprotection. We hypothesized that other noble gases without anesthetic properties [helium (He), neon (Ne), argon (Ar)] also produce cardioprotection, and further hypothesized that this beneficial effect is mediated by activation of
Postconditioning of sevoflurane and propofol is associated with mitochondrial permeability transition pore.
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BACKGROUND
Sevoflurane and propofol are effective cardioprotective anaesthetic agents, though the cardioprotection of propofol has not been shown in humans. Their roles and underlying mechanisms in anesthetic postconditioning are unclear. Mitochondrial permeability transition pore (MPTP) opening is
Hydroxytyrosol protects against myocardial ischemia reperfusion injury by inhibiting mitochondrial permeability transition pore opening.
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Hydroxytyrosol (HT), a phenolic compound extracted from olive oil, is reported to protect against myocardial ischemia reperfusion injury (MIRI), but its mechanism has not been fully elucidated. The mitochondria permeability transition pore (MPTP) is an important therapeutic target for MIRI. The
The mitochondrial permeability transition pore and the Ca2+-activated K+ channel contribute to the cardioprotection conferred by tumor necrosis factor-alpha.
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Pretreatment with tumor necrosis factor-alpha (TNF-alpha) is known to trigger cardioprotection and it can activate multiple downstream signaling cascades. However, it is not known whether the mitochondrial permeability transition pore and the Ca(2+)-activated K(+) channel (K(Ca) channel) are
Antioxidant MCI-186 inhibits mitochondrial permeability transition pore and upregulates Bcl-2 expression.
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Reperfusion after a period of ischemia is associated with the formation of reactive oxygen species (ROS) and Ca2+ overload resulting in the opening of a nonspecific pore in the inner membrane of the mitochondria, called the mitochondrial permeability transition pore (PTP), leading to cell damage.
Novel bisindolylmaleimide derivative inhibits mitochondrial permeability transition pore and protects the heart from reperfusion injury.
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Despite major advances in treating patients with coronary heart disease, reperfusion injury is still considered to be a major problem, especially in surgical settings. Here, we demonstrate the protective effects of a novel bisindolylmaleimide derivative, MS1
Delayed cardioprotection afforded by the glycogen synthase kinase 3 inhibitor SB-216763 occurs via a KATP- and MPTP-dependent mechanism at reperfusion.
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Previous studies in our laboratory suggest that an acute inhibition of glycogen synthase kinase 3 (GSK3) by SB-216763 (SB21) is cardioprotective when administered just before reperfusion. However, it is unknown whether the GSK inhibitor SB21 administered 24 h before ischemia is cardioprotective and
Postconditioning with sevoflurane protects against focal cerebral ischemia and reperfusion injury involving mitochondrial ATP-dependent potassium channel and mitochondrial permeability transition pore.
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OBJECTIVE
Postconditioning with sevoflurane has been shown to protect against focal cerebral ischemia and reperfusion injury. However, the mechanism remains elusive. In this study, we tested the hypothesis that mitochondrial ATP-sensitive potassium (mitoKATP) and mitochondrial permeability
Calcium-activated potassium channel triggers cardioprotection of ischemic preconditioning.
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We tested the hypothesis that the high-conductance calciumactivated potassium (K(Ca)) channel is involved in the cardioprotection of preconditioning with ischemic insults. In the isolated perfused rat heart subjected to ischemia/reperfusion, effects of ischemic preconditioning (IPC) on infarct size
Vasopressin attenuates ischemia-reperfusion injury via reduction of oxidative stress and inhibition of mitochondrial permeability transition pore opening in rat hearts.
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Aim of this study was to investigate the involvement of the mitochondrial permeability transition pore (MPTP) and oxidative stress in the cardioprotective effect of vasopressin (AVP) on ischemia/reperfusion (I/R) injury. Anesthetized male wistar rats were subjected to regional 30 min ischemia and
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