α2A-adrenergic blockade attenuates septic cardiomyopathy by increasing cardiac norepinephrine concentration and inhibiting cardiac endothelial activation.

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α2A-adrenergic blockade attenuates septic cardiomyopathy by increasing cardiac norepinephrine concentration and inhibiting cardiac endothelial activation.

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2018 nî lūn-bûn

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2018年の論文

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2018年学术文章

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2018年学术文章

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2018年学术文章

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2018年学术文章

@zh-my

2018年学术文章

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2018年學術文章

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2018年學術文章

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2018年學術文章

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name

α2A-adrenergic blockade attenu ...... ardiac endothelial activation.

@en

α2A-adrenergic blockade attenu ...... ardiac endothelial activation.

@nl

type

Item

label

α2A-adrenergic blockade attenu ...... ardiac endothelial activation.

@en

α2A-adrenergic blockade attenu ...... ardiac endothelial activation.

@nl

prefLabel

α2A-adrenergic blockade attenu ...... ardiac endothelial activation.

@en

α2A-adrenergic blockade attenu ...... ardiac endothelial activation.

@nl

P1476

α2A-adrenergic blockade attenu ...... ardiac endothelial activation.

@en

P2093

Ben Lv

http://www.w3.org/2001/XMLSchema#string

Chaofeng Hu

http://www.w3.org/2001/XMLSchema#string

Daxiang Lu

http://www.w3.org/2001/XMLSchema#string

Duomeng Yang

http://www.w3.org/2001/XMLSchema#string

Hongmei Li

http://www.w3.org/2001/XMLSchema#string

Huadong Wang

http://www.w3.org/2001/XMLSchema#string

Renbin Qi

http://www.w3.org/2001/XMLSchema#string

Xiangxu Tang

http://www.w3.org/2001/XMLSchema#string

Xiaohui Yu

http://www.w3.org/2001/XMLSchema#string

Xiuxiu Lv

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P2860

A comparative study of the reversal by different alpha 2-adrenoceptor antagonists of the central sympatho-inhibitory effect of clonidine

Antagonism of alpha2A-adrenoceptor: a novel approach to inhibit inflammatory responses in sepsis

Cardiac contractile impairment associated with increased phosphorylation of troponin I in endotoxemic rats.

Caspase inhibition prevents cardiac dysfunction and heart apoptosis in a rat model of sepsis.

Pivotal role of the alpha(2A)-adrenoceptor in producing inflammation and organ injury in a rat model of sepsis

Yohimbine promotes cardiac NE release and prevents LPS-induced cardiac dysfunction via blockade of presynaptic α2A-adrenergic receptor

MyD88 and Trif signaling play distinct roles in cardiac dysfunction and mortality during endotoxin shock and polymicrobial sepsis.

β₁-adrenoceptor stimulation promotes LPS-induced cardiomyocyte apoptosis through activating PKA and enhancing CaMKII and IκBα phosphorylation.

Sepsis-induced cardiomyopathy.

Toll-like receptor 3 plays a central role in cardiac dysfunction during polymicrobial sepsis.

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5478

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scholarly article

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10.1038/S41598-018-23304-7

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English

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P478

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2018-04-03T00:00:00Z

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29615637

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P921

norepinephrine

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5882799

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