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Myocardial dysfunction in donor hearts. A possible etiology

V J Owen1, P B Burton, M C Michel

  • 1Cardiothoracic Surgery, National Heart and Lung Institute at Imperial College School of Medicine, London, UK. v.j.owen@ic.ac.uk

Circulation
|May 20, 1999
PubMed

Insights

Increased inhibitory G protein Gialpha activity contributes to impaired contractility in acutely failing donor hearts. This contrasts with changes in calcium-handling proteins and beta-adrenoceptor density, which were not common causes.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Transplantation Science

Background:

  • Unused donor hearts often exhibit myocardial dysfunction, rendering them unsuitable for transplantation.
  • The underlying mechanisms of acute heart failure in these hearts remain unclear.
  • This study investigates potential causes including calcium-handling proteins, beta-adrenoceptor density, and inhibitory G protein Gialpha.

Purpose of the Study:

  • To determine the molecular basis of contractile dysfunction in acutely failing donor hearts.
  • To compare alterations in unused donor hearts with those in end-stage failing and nonfailing hearts.
  • To identify key protein targets contributing to impaired cardiac function.

Main Methods:

  • Analysis of myocardial samples from unused donor hearts (ejection fraction <30%), end-stage failing hearts, and nonfailing hearts.
  • In vitro assessment of inotropic function in trabeculae and isolated myocytes.
  • Quantification of specific calcium-handling proteins (SERCA, NCX), beta-adrenoceptor density, and Gialpha activity.

Main Results:

  • Unused donor hearts showed contractile dysfunction comparable to failing hearts.
  • Alterations in sarcoplasmic reticulum calcium-ATPase and sodium-calcium exchanger abundance were not common to both groups.
  • Beta-adrenoceptor density was reduced in failing hearts but not in unused donor hearts.
  • Increased inhibitory G protein Gialpha activity was observed in both unused donor and failing hearts.

Conclusions:

  • Elevated Gialpha activity is a significant factor in the impaired contractility of acutely failing donor hearts.
  • This finding differentiates the mechanism from alterations in calcium-handling proteins or beta-adrenoceptor density.
  • Targeting Gialpha may offer therapeutic potential for preserving cardiac function in donor hearts.
Abstract

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