HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Thomas Yeh, Jr Andrew S. Wechsler Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Yeh, T. Articles by Jakoi, E. R. Search for Related Content PubMed PubMed Citation Articles by Yeh, T., Jr Articles by Jakoi, E. R. Related Collections Molecular biology Transplantation - heart

J Thorac Cardiovasc Surg 2002;124:1087-1098
© 2002 The American Association for Thoracic Surgery

Cardiopulmonary Support and Physiology (CSP)

Central sympathetic blockade ameliorates brain death-induced cardiotoxicity and associated changes in myocardial gene expression

From the Jewish Hospital Cardiovascular Research Center at University of Louisville, Department of Surgery,^a Division of Cardiothoracic Surgery, University of Louisville, Louisville, Ky, Department of Cell Biology,^b Duke University, Durham, NC, Department of Cardiothoracic Surgery,^c MCP Hahnemann University, Philadelphia, Pa, Department of Biological Sciences,^d Mary Washington College, Fredericksburg, Va, and Departments of Surgery^e and Medicine,^f Medical College of Virginia, Richmond, Va.

Supported in part by grants from the United States Public Health Service (grant GM3529 [E.R.J.], the National Institutes of Health (grant HL26302 [ASW]), and the American Heart Association (grant AHA94010440 [ASW]).

Received for publication Aug 8, 2001. Revisions requested Dec 11, 2001; revisions received Jan 28, 2002. Accepted for publication Feb 4, 2002. Address for reprints: Thomas Yeh, Jr, MD, PhD, Department of Surgery, Division of Cardiothoracic Surgery, University of Louisville, Jewish Hospital Cardiovascular Research Center, 201 Abraham Flexner Way, Suite 1200, Louisville, KY 40202.

Objective: Brain death results in cardiac injury and hemodynamic instability. After brain death, catecholamine levels surge in concert with increased expression of select myocardial gene products. Sympathetic blockade was used to investigate the effects of the adrenergic nervous system on myocardial gene expression in a rabbit model of brain death.
Methods: A balloon expansion model of brain death in rabbits (n = 42) was used with and without sympathetic blockade (xylazine, acetylpromazine, and ketamine). Sham-operated and naive rabbits served as control animals. Over 4 hours, mean arterial pressure, heart rate, electrocardiographic results, catecholamine levels, myocardial histology, and messenger RNA levels were assessed.
Results: Sympathetic blockade decreased basal catecholamine levels and blocked the catecholamine surge accompanying brain death. The typical hemodynamic instability, adverse electrocardiographic changes, and myocellular injury associated with brain death were all significantly decreased. Sympathetic blockade not only suppressed the previously reported increases in myocardial gene expression (cardiac and skeletal -actin, egr-1, and heat shock protein 70) but also suppressed the expression of multiple other genes ( and ß myosin heavy chain, calcium ATPase [sarcoplasmic reticulum Ca²⁺-adenosine triphosphatase pump, SERCA-2a], phospholamban [ryanodine receptor], and c-jun).
Conclusion: Central sympathetic blockade minimizes the hemodynamic instability associated with brain death and neutralizes the increased expression of multiple myocardial gene products associated with brain death.

This article has been cited by other articles:

				A. H. Harken Brain death leads to abnormal contractile properties of the human donor right ventricle J. Thorac. Cardiovasc. Surg., July 1, 2006; 132(1): 10 - 11. [Full Text] [PDF]