gms | German Medical Science

27. Wissenschaftlicher Kongress der Deutschen Hochdruckliga

Deutsche Liga zur Bekämpfung des hohen Blutdrucks – Deutsche Hypertonie Gesellschaft e. V.

26. bis 29.11.2003, Bonn

Metabolic changes following acute myocardial infarction are partially reversed after treatment with the ACE inhibitor quina

Metabolische Veränderungen nach akutem Myocardinfarkt werden teilweise durch Behandlung mit dem ACE Hemmer Quinapril aufgehoben

Meeting Abstract (Hypertonie 2003)

  • presenting/speaker D. Westermann
  • A. Riad
  • V. Regitz-Zagrosek
  • C. Tschöpe
  • J. Fielitz

Hypertonie 2003. 27. Wissenschaftlicher Kongress der Deutschen Hochdruckliga. Bonn, 26.-29.11.2003. Düsseldorf, Köln: German Medical Science; 2004. Doc03hochP75

Die elektronische Version dieses Artikels ist vollständig und ist verfügbar unter: http://www.egms.de/de/meetings/hoch2003/03hoch175.shtml

Veröffentlicht: 11. November 2004

© 2004 Westermann et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielf&aauml;ltigt, verbreitet und &oauml;ffentlich zug&aauml;nglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Acute myocardial infarction (AMI) leads to metabolic changes in the infarcted and non-infarcted myocardium. ACE inhibitor therapy reduces left ventricular (LV) remodeling and scar formation and could therefore have an impact on infarct associated metabolic changes. PPARα and carnitine palmitoyltransferase-I (CPT-I) play an important role in cardiac fatty acid import and oxidation, (FAO) and have been implicated in the development of cardiac dysfunction. GLUT4 is a key receptor for insulin-mediated myocardial glucose uptake.

We investigated metabolic changes following AMI and interaction of the ACE inhibitor quinapril (Qui) with PPARα, CPT-I and GLUT4 mRNA in the infarcted region of the LV from Sprague Dawley rats. 8 week old rats were either sham operated (n=6) or received AMI by LAD ligation. From day 2 to day 21 AMI rats received Qui (n=6; 10mg/kg Bwt/die) or vehicle (n=6). At the end of the study, LV function was determined using a Millar Tip catheter. Finally, hearts were excided and divided into infracted (Inf) and non-infarcted (Non-Inf) region and further analysed for PPARα, CPT-I and GLUT4 mRNA expression by real-time PCR (TaqMan®).

LV function was improved to 35% after Qui treatment compared to controls with respect to LV pressure, dP/dt max. and min, and enddiastolic pressure. LV PPARα and CPT-I mRNA levels were significantly decreased in Inf. and Non-inf. GLUT4 mRNA was only downregulated in Inf but unchanged in Non-inf. Qui reversed changes in PPARα and GLUT4 in the infracted region [Tab. 1].

AMI impairs metabolic switching by PPARα, FAO and insulin stimulated glucose uptake in the infarcted region and PPARα and FAO in the non-infarcted myocardial region. ACE inhibition reverse metabolic switching in the infracted myocardium what may contribute to their beneficial effect in AMI.