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Updated: Aug 14, 2026
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Gene Transfer for Ischemic Heart Failure in a Preclinical Model
Published on: May 15, 2011
Acute brain death alters left ventricular myocardial gene expression
T Yeh1, A S Wechsler, L J Graham
1Department of Surgery, University of Louisville, Ky 40202, USA.
The Journal of Thoracic and Cardiovascular Surgery
|January 27, 1999
Summary
Acute brain death alters myocardial gene expression, leading to ventricular remodeling and dysfunction. This study in rabbits shows increased intracranial pressure affects genes crucial for heart contractility.
Area of Science:
- Cardiovascular Physiology
- Molecular Biology
- Neurocritical Care
Background:
- Brain death is associated with myocardial dysfunction, often attributed to sympathetic overactivity and catecholamine toxicity.
- Elevated catecholamines can alter myocardial gene expression, potentially contributing to cardiac dysfunction.
Purpose of the Study:
- To investigate if acute brain death induced by increased intracranial pressure alters myocardial gene expression.
- To identify specific genes involved in myocardial contractility affected by brain death.
Main Methods:
- Rabbits underwent induced brain death via increased intracranial pressure using a balloon expansion model.
- Systemic hemodynamics, catecholamine levels, and myocardial gene expression (mRNA) were assessed at timed intervals.
- Histologic myocardial injury was evaluated to correlate with molecular changes.
Main Results:
- Increased intracranial pressure caused immediate pressor response and ST segment changes, with transiently elevated catecholamines.
- Histologic myocardial injury was observed within 1 hour.
- Four hours post-brain death, significant increases in mRNA for skeletal/cardiac alpha-actins, egr-1, and heat shock protein 70 were detected.
Conclusions:
- Acute brain death triggers specific changes in myocardial gene expression.
- These gene expression alterations suggest ventricular remodeling contributes to myocardial dysfunction in acute brain death.
