Impairment of beta-adrenergic receptor signalling as a cause of both pulmonary oedema and cardiovascular failure in patients with septicaemia.
作者信息
Eisenhut Michael
出版信息
Pathology. 2007 Dec;39(6):611-2. doi: 10.1080/00313020701684433.
PMID:18027273
Abstract
摘要
相似文献
1
Impairment of beta-adrenergic receptor signalling as a cause of both pulmonary oedema and cardiovascular failure in patients with septicaemia.
Pathology. 2007 Dec;39(6):611-2. doi: 10.1080/00313020701684433.
2
The involvement of nitric oxide and beta-adrenergic pathway signalling in pulmonary oedema and fluid clearance.一氧化氮和β-肾上腺素能通路信号在肺水肿及液体清除中的作用
Pathology. 2007 Dec;39(6):612-3. doi: 10.1080/00313020701684441.
3
Novel insights into the effects of inducible nitric oxide synthase inhibition during sepsis.
Crit Care Med. 2008 Jan;36(1):359-60. doi: 10.1097/01.CCM.0000297947.51539.8F.
4
Signal transduction mechanisms controlling cardiac contractility and their alterations in chronic heart failure.控制心脏收缩力的信号转导机制及其在慢性心力衰竭中的改变。
Cardiovasc Res. 1995 Oct;30(4):570-84.
5
Modulation of the myocardial redox state by vagal nerve stimulation after experimental myocardial infarction.实验性心肌梗死后迷走神经刺激对心肌氧化还原状态的调节作用。
Cardiovasc Res. 2008 Mar 1;77(4):713-21. doi: 10.1093/cvr/cvm092. Epub 2007 Dec 7.
6
Toll-like receptors and myocardial contractile dysfunction.
Cardiovasc Res. 2008 Apr 1;78(1):3-4. doi: 10.1093/cvr/cvn044. Epub 2008 Feb 15.
7
Beta-adrenergic receptors signaling and heart failure in mice, rabbits and humans.小鼠、兔子和人类中的β-肾上腺素能受体信号传导与心力衰竭
J Mol Cell Cardiol. 2006 Jul;41(1):11-3. doi: 10.1016/j.yjmcc.2006.04.001. Epub 2006 May 23.
8
[Beta-adrenergic receptors in normal and failing heart].[正常及衰竭心脏中的β-肾上腺素能受体]
Kardiol Pol. 2007 Mar;65(3):294-302.
9
Nitric oxide mechanisms of nebivolol.奈必洛尔的一氧化氮机制。
Ther Adv Cardiovasc Dis. 2009 Aug;3(4):317-27. doi: 10.1177/1753944709104496. Epub 2009 May 14.
10
Elevated sweat sodium associated with pulmonary oedema in meningococcal sepsis.
Eur J Clin Invest. 2004 Aug;34(8):576-9. doi: 10.1111/j.1365-2362.2004.01386.x.
引用本文的文献
1
Overexpression of Hsp20 prevents endotoxin-induced myocardial dysfunction and apoptosis via inhibition of NF-kappaB activation.热休克蛋白20（Hsp20）的过表达通过抑制核因子κB（NF-κB）的激活来预防内毒素诱导的心肌功能障碍和细胞凋亡。
J Mol Cell Cardiol. 2009 Sep;47(3):382-90. doi: 10.1016/j.yjmcc.2009.05.016. Epub 2009 Jun 6.
Zotero 插件