Myocardial edema: a translational view

J Mol Cell Cardiol. 2012 May;52(5):931-9. doi: 10.1016/j.yjmcc.2012.01.010. Epub 2012 Jan 18.

Abstract

Myocardial edema occurs in a large number of myocardial pathologies particularly during ischemia-reperfusion, and may contribute to cell dysfunction and death occurring in these conditions. Cardiomyocyte cell volume is tightly regulated by modifications in cytosolic osmolality. Changes in membrane water permeability through aquaporin and connexin hemichannels also contribute to cell volume changes while caveolae may be important in sensing cell volume changes sensing and associated signaling. Ischemia-reperfusion alters these mechanisms and increases microvascular permeability by endothelial hypercontracture-induced gap formation, endothelial cell death and basal membrane disruption. Detection of myocardial edema by MRI has many useful diagnostic applications in acute myocardial infarction and other conditions. However, discrimination between intra and extracellular myocardial edema is presently difficult at the bench and impossible at the bedside. Developing methods to differentiate intra from extracellular myocardial water should allow a better understanding of the mechanisms and consequences of myocardial edema and, as a consequence lead to new diagnostic and therapeutic applications.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Aquaporins / metabolism
  • Aquaporins / physiology
  • Cell Enlargement
  • Cell Size
  • Edema, Cardiac / etiology
  • Edema, Cardiac / metabolism
  • Edema, Cardiac / pathology*
  • Humans
  • Myocardial Reperfusion Injury / complications
  • Myocardial Reperfusion Injury / metabolism
  • Myocardial Reperfusion Injury / pathology
  • Myocytes, Cardiac / metabolism
  • Myocytes, Cardiac / physiology
  • Osmotic Pressure
  • Translational Medical Research

Substances

  • Aquaporins