Response of hypertrophied myocardium to ischemia: correlation with biochemical and physiological parameters.

Published

Journal Article

The increased susceptibility of hypertrophied hearts to ischemic injury during cardiac operations has long been recognized. Although the imbalances in oxygen supply and demand which may occur with hypertrophy during hypotension, ventricular fibrillation, or reperfusion have been extensively studied, the biochemical response of hypertrophied myocardium to ischemia has not been fully elucidated. In the present investigation, rat hearts in which hypertrophy was induced by chronic pressure overload were used to examine the relationship of the physiological parameter, ischemic contracture, to high-energy phosphate content and mitochondrial function during global ischemia. Hypertrophied hearts developed ischemic contracture after significantly shorter duration of ischemia than did normal hearts (5.8 +/- 0.3 minutes versus 10.1 +/- 0.7 minutes). High-energy phosphate content was lower in hypertrophied hearts at control and at ischemic contracture initiation and completion than in normal hearts, whereas mitochondrial function was consistently greater in the hypertrophy group. This investigation demonstrates that the hypertrophied myocardium, independent of flow-related events, is more vulnerable to ischemic injury than normal myocardium and suggests that the increased susceptibility may result from lower high-energy phosphate stores present at the onset of ischemia. The results emphasize the need for rapid cardiac arrest with the induction of ischemia in hypertrophied myocardium and suggest the potential for increasing myocardial high-energy phosphate content in the hypertrophied ventricle by interventions such as arrested perfusion with substrate containing oxygenated cardioplegic solutions prior to the onset of planned ischemia.

Full Text

Duke Authors

Cited Authors

  • Sink, JD; Pellom, GL; Currie, WD; Hill, RC; Olsen, CO; Jones, RN; Wechsler, AS

Published Date

  • June 1981

Published In

Volume / Issue

  • 81 / 6

Start / End Page

  • 865 - 872

PubMed ID

  • 6453258

Pubmed Central ID

  • 6453258

International Standard Serial Number (ISSN)

  • 0022-5223

Language

  • eng

Conference Location

  • United States