English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Myocardial stunning1 and hibernation2 have been subjects of intense laboratory and clinical investigations to elucidate mechanisms responsible for contractile dysfunction after transient ischemia or chronic hypoperfusion. Considerable evidence has implicated the generation of oxygen-derived free radicals and derangements in myocardial energy metabolism and excitation-contraction coupling as major contributors to the pathogenesis of myocardial stunning and hibernation.3 4 Despite enormous progress in this area, however, our understanding of the cellular pathophysiology of contractile dysfunction in ischemic heart disease remains incomplete.In this issue of Circulation , Kaprielian et al5 provide evidence for a novel mechanism involving alterations in intercellular coupling that might contribute to the pathogenesis of contractile dysfunction in hibernating myocardium. Using digital image processing techniques and confocal immunofluorescence microscopy, they measured the amount of the major cardiac gap junction protein connexin43 (Cx43) in left ventricular samples obtained from patients at the time of coronary artery bypass graft surgery. Biopsies were taken from well perfused, normally contracting wall segments (identified with preoperative thallium scans and magnetic resonance imaging studies) and from “reversibly ischemic” segments (showing improved thallium uptake on stress/redistribution images but no improvement in contractile function after revascularization) or “hibernating” segments (showing improved contractile performance in postoperative MRI studies). Mean gap junction area, determined by measuring the amount of Cx43 immunoreactive signal at intercellular junctions and expressed per unit of intercalated disk area, was reduced by ≈23% in reversibly ischemic segments and by 33% in hibernating tissue compared with normally perfused regions. The average size of an individual gap junction was also reduced by 13% and 30% in reversibly ischemic and hibernating regions, respectively, due mainly to loss of the largest gap junctions in myocytes of dysfunctional regions. The authors suggest, on the basis of these observations, that reduction of Cx43 content in gap junctions …

Do Alterations in Intercellular Coupling Play a Role in Cardiac Contractile Dysfunction?