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7 results on '"Qi, Renbin"'

1. The Effects of Chloroquine and Hydroxychloroquine on ACE2-Related Coronavirus Pathology and the Cardiovascular System: An Evidence-Based Review

Author

Chen, Li, primary, Chen, Haiyan, additional, Dong, Shan, additional, Huang, Wei, additional, Chen, Li, additional, Wei, Yuan, additional, Shi, Liping, additional, Li, Jinying, additional, Zhu, Fengfeng, additional, Zhu, Zhu, additional, Wang, Yiyang, additional, Lv, Xiuxiu, additional, Yu, Xiaohui, additional, Li, Hongmei, additional, Wei, Wei, additional, Zhang, Keke, additional, Zhu, Lihong, additional, Qu, Chen, additional, Hong, Jian, additional, Hu, Chaofeng, additional, Dong, Jun, additional, Qi, Renbin, additional, Lu, Daxiang, additional, Wang, Huadong, additional, Peng, Shuang, additional, and Hao, Guang, additional

Published
2020
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7. α 2A -adrenergic blockade attenuates septic cardiomyopathy by increasing cardiac norepinephrine concentration and inhibiting cardiac endothelial activation.

Author

Yu X, Wang Y, Yang D, Tang X, Li H, Lv X, Qi R, Hu C, Lu D, Lv B, and Wang H

Subjects
Adrenergic alpha-2 Receptor Antagonists therapeutic use, Animals, Apoptosis drug effects, Cardiomyopathies complications, Cardiomyopathies pathology, Cardiomyopathies physiopathology, Dose-Response Relationship, Drug, Endothelial Cells metabolism, Endothelial Cells pathology, Gene Deletion, Gene Expression Regulation drug effects, Heart drug effects, Heart physiopathology, JNK Mitogen-Activated Protein Kinases metabolism, Male, Myocardium pathology, NF-KappaB Inhibitor alpha metabolism, Neutrophil Infiltration drug effects, Phosphorylation drug effects, Rats, Rats, Sprague-Dawley, Receptors, Adrenergic, alpha-2 deficiency, Receptors, Adrenergic, alpha-2 genetics, Survival Analysis, Tumor Necrosis Factor-alpha biosynthesis, Vascular Cell Adhesion Molecule-1 metabolism, Ventricular Function, Left drug effects, p38 Mitogen-Activated Protein Kinases metabolism, Adrenergic alpha-2 Receptor Antagonists pharmacology, Cardiomyopathies drug therapy, Endothelial Cells drug effects, Myocardium metabolism, Norepinephrine metabolism, Receptors, Adrenergic, alpha-2 metabolism, Sepsis complications
Abstract

Cardiomyopathy is a common complication associated with increased mortality in sepsis, but lacks specific therapy. Here, using genetic and pharmacological approaches, we explored the therapeutic effect of α 2A -adrenergic receptor (AR) blockade on septic cardiomyopathy. CLP-induced septic rats were treated with BRL44408 (α 2A -AR antagonist), prazosin (α 1 -AR antagonist) and/or reserpine. CLP-induced cardiomyopathy, indicated by reduced dP/dt and increased cardiac troponin I phosphorylation, was attenuated by BRL44408, this was associated with reduced cardiac TNF-α and endothelial VCAM-1 expression, cardiomyocyte apoptosis and related signal molecule phosphorylation. BRL44408 increased cardiac norepinephrine (NE) concentration in CLP rats. Pretreatment with reserpine that exhausts cardiac NE without affecting the circulating NE concentration or with prazosin partially abolished the cardioprotection of BRL44408 and reversed its inhibitory effects on myocardial TNF-α, apoptosis and related signal molecule phosphorylation, but not on VCAM-1 expression in septic rats. These effects of BRL44408 were confirmed by α 2A -AR gene deletion in septic mice. Furthermore, α 2 -AR agonist not only enhanced LPS-induced TNF-α and VCAM-1 expression in cardiac endothelial cells that express α 2A -AR, but also enhanced LPS-induced cardiac dysfunction in isolated rat hearts. Our data indicate that α 2A -AR blockade attenuates septic cardiomyopathy by promoting cardiac NE release that activates myocardial α 1 -AR and suppressing cardiac endothelial activation.

Published
2018
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