Selective β 2 -Adrenoreceptor Stimulation Attenuates Myocardial Cell Death and Preserves Cardiac Function After Ischemia–Reperfusion Injury | Zendy

Shashi Bhushan | Zendy; Kazuhisa Kondo | Zendy; Benjamin L. Predmore | Zendy; Maxim Zlatopolsky | Zendy; Adrienne L. King | Zendy; Claire Pearce | Zendy; Hui Huang | Zendy; YaXiong Tao | Zendy; Marah E. Condit | Zendy; David J. Lefer | Zendy

Open Access

Selective β ₂ -Adrenoreceptor Stimulation Attenuates Myocardial Cell Death and Preserves Cardiac Function After Ischemia–Reperfusion Injury

Author(s) -

Shashi Bhushan,

Kazuhisa Kondo,

Benjamin L. Predmore,

Maxim Zlatopolsky,

Adrienne L. King,

Claire Pearce,

Hui Huang,

YaXiong Tao,

Marah E. Condit,

David J. Lefer

Publication year - 2012

Publication title -

arteriosclerosis thrombosis and vascular biology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.007

H-Index - 270

eISSN - 1524-4636

pISSN - 1079-5642

DOI - 10.1161/atvbaha.112.251769

Subject(s) - medicine , enos , protein kinase b , cardioprotection , reperfusion injury , myocardial infarction , stimulation , endocrinology , ischemia , troponin i , troponin t , ejection fraction , cardiology , phosphorylation , heart failure , nitric oxide synthase , chemistry , nitric oxide , biochemistry

β(2)-adrenoreceptor activation has been shown to protect cardiac myocytes from cell death. We hypothesized that acute β(2)-adrenoreceptor stimulation, using arformoterol (ARF), would attenuate myocardial ischemia/reperfusion (R) injury via NO synthase activation and cause a subsequent increase in NO bioavailability.

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