IMR Press / FBL / Volume 12 / Issue 8 / DOI: 10.2741/2294

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article
Apoptotic cardiomyocyte hypertrophy during sepsis and septic shock results from prolonged exposure to endothelin precursor
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1 Cardionome Laboratory, The Texas A&M University System Health Science Center, Baylor College of Dentistry, Department of Biomedical Sciences, Dallas, TX 75246, USA
Academic Editor:Pudur Jagadeeswaran
Front. Biosci. (Landmark Ed) 2007, 12(8), 3052–3060; https://doi.org/10.2741/2294
Published: 1 May 2007
(This article belongs to the Special Issue The zebrafish as a model for human disease)
Abstract

Septic shock is a complex cardiovascular dysfunction which leads to regional circulatory alterations and multi-organ dysfunction in humans and animal models. To elucidate the role of stress-activated signaling molecules in the regulation of myocardial dysfunction, we have developed and standardized isolated ventricular myocyte techniques. These techniques allow the assessment of cardiodynamics at cellular (ventricular myocyte) level. These studies are carried out in a well defined model of systemic inflammatory response syndrome following polymicrobial sepsis in the rat. Evidence is provided that sepsis-induced myocardial dysfunction produces indications (signs) of early stages of heart failure. This evidence correlates with upregulation of stress-activated protein kinase cascade. These findings suggest that prolonged exposure to endothelin precursor causes decompensatory hypertrophy in adult rat ventricular myocytes (ARVMs) during sepsis. The decompensatory hypertrophy could, in turn, results in increased cytosolic caspases-3 activity in ARVMs.

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