If you are experiencing problems downloading PDF or HTML fulltext, our helpdesk recommend clearing your browser cache and trying again. If you need help in clearing your cache, please click here . Still need help? Email help@ingentaconnect.com

Cardiac accumulation of citrate during brief myocardial ischaemia and reperfusion in the pig in vivo

$48.00 plus tax (Refund Policy)

Download / Buy Article:

Abstract:

Citrate is a key intermediate in energy metabolism and an inhibitor of phosphofructokinase of the glycolytic pathway. During myocardial ischaemia glycolysis is the main source of cardiac ATP. The aim of the present study was to determine if myocardial ischaemia and reperfusion alter cardiac tissue levels of citrate. Open-chest, anaesthetized pigs were subjected to 10 min of regional myocardial ischaemia by occlusion of the left anterior descending coronary artery, with and without reperfusion, and to 10 min of global ischaemia by circulatory arrest. Citrate, amino acids, glucose and NH3 were measured in biopsies. Ischaemia, whether regional or global, caused a 60–70% increase in tissue levels of citrate. During 1 min of reperfusion following regional ischaemia the level of citrate increased 460%, to ≈600 nmol g−1 wet weight. The level of glutamate decreased by 20–33% (corresponding to 1300–2200 nmol g−1 wet weight), indicating net consumption of this amino acid during ischaemia. The level of aspartate decreased 50% indicating conversion of aspartate to oxaloacetate for the synthesis of citrate. Theoretically, the accumulation of myocardial citrate during brief ischaemia and early reperfusion is large enough to significantly inhibit phosphofructokinase activity and could therefore affect the ability of the myocardium to increase the glycolytic rate in response to ischaemia. This could, however, be partly compensated by the metabolism of myocardial glutamate.

Keywords: alanine; citrate; glutamate; glycolysis; myocardial ischaemia; reperfusion

Document Type: Original Article

DOI: http://dx.doi.org/10.1046/j.1365-201X.1998.0400e.x

Affiliations: 1: Norwegian Defence Research Establishment, Division for Environmental Toxicology, Kjeller, Norway 2: Institute for Experimental Medical Research, Ullevål Hospital, Oslo, Norway

Publication date: September 1, 1998

Related content

Tools

Favourites

Share Content

Access Key

Free Content
Free content
New Content
New content
Open Access Content
Open access content
Subscribed Content
Subscribed content
Free Trial Content
Free trial content
Cookie Policy
X
Cookie Policy
ingentaconnect website makes use of cookies so as to keep track of data that you have filled in. I am Happy with this Find out more