K(ATP) channel opening is an endogenous mechanism of protection against the no-reflow phenomenon but its function is compromised by hypercholesterolemia.
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No-Reflow Phoenomenon by Intracoronary Thrombus in Acute Myocardial InfarctionPretreatment with simvastatin reduces myocardial no-reflow by opening mitochondrial K(ATP) channelEstablishment and characterization of an experimental model of coronary thrombotic microembolism in rats.Cholesterol down-regulates BK channels stably expressed in HEK 293 cells.Identification of a binding motif in the S5 helix that confers cholesterol sensitivity to the TRPV1 ion channel.Cardiac microvascular barrier function mediates the protection of Tongxinluo against myocardial ischemia/reperfusion injury.The role of von Willebrand factor and ADAMTS13 in the no-reflow phenomenon: after primary percutaneous coronary interventionMicrovascular alterations after temporary coronary artery occlusion: the no-reflow phenomenon.Pharmacological preconditioning and postconditioning with nicorandil attenuates ischemia/reperfusion-induced myocardial necrosis and apoptosis in hypercholesterolemic ratsEffects of exercise training and hypercholesterolemia on adenosine activation of voltage-dependent K+ channels in coronary arterioles.Effects of intravenous diltiazem in a rat model of experimental coronary thrombotic microembolism.Cholesterol and Kir channels.Ischemic preconditioning: Interruption of various disorders.Regulation of ion channels by membrane lipids.Mechanisms involved in attenuated cardio-protective role of ischemic preconditioning in metabolic disorders.Comparative analysis of cholesterol sensitivity of Kir channels: role of the CD loop.Optimal therapeutic strategies in the setting of post-infarct no reflow: the need for a pathogenetic classification.Matter of Fat: Are Lipids Antiarrhythmic?Cholesterol-enriched diet inhibits cardioprotection by ATP-sensitive K+ channel activators cromakalim and diazoxide.Carvedilol reduces myocardial no-reflow by decreasing endothelin-1 via activation of the ATP-sensitive K+ channel.Postconditioning fails to improve no reflow or alter infarct size in an open-chest rabbit model of myocardial ischemia-reperfusion.Serum N-terminal pro-B-type natriuretic peptide levels at the time of hospital admission predict of microvascular obstructions after primary percutaneous coronary intervention for acute ST-segment elevation myocardial infarction.
P2860
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P2860
K(ATP) channel opening is an endogenous mechanism of protection against the no-reflow phenomenon but its function is compromised by hypercholesterolemia.
description
2002 nî lūn-bûn
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2002年の論文
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2002年学术文章
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2002年学术文章
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2002年学术文章
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name
K(ATP) channel opening is an e ...... mised by hypercholesterolemia.
@en
type
label
K(ATP) channel opening is an e ...... mised by hypercholesterolemia.
@en
prefLabel
K(ATP) channel opening is an e ...... mised by hypercholesterolemia.
@en
P2093
P1476
K(ATP) channel opening is an e ...... mised by hypercholesterolemia.
@en
P2093
Kazuaki Shimamoto
Satoshi Genda
Takayuki Miki
Tetsuji Miura
Yoshihiko Ichikawa
P304
P356
10.1016/S0735-1097(02)02156-3
P407
P577
2002-10-01T00:00:00Z