Apoptotic cardiomyocyte hypertrophy during sepsis and septic shock results from prolonged exposure to endothelin precursor

Document Type

Article

Publication Date

2007

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.

Publication Title

Frontiers in Bioscience

Volume

12

Issue

8

First Page

3052

Last Page

3060

Comments

This article was published in Frontiers in Bioscience, Volume 12, Issue 8, Pages 3052-3060.

The published version is available at http://dx.doi.org/10.2741/2294.

Copyright © 2007 Frontiers in BioScience.

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