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This Article Full Text Full Text (PDF) All Versions of this Article: 89/5/605    most recent expphysiol.2004.027649v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by De Celle, T. Articles by Janssen, B. J. Search for Related Content PubMed PubMed Citation Articles by De Celle, T. Articles by Janssen, B. J. Related Collections Heart/Cardiac Muscle

Departments of ¹ Pharmacology & Toxicology² Pathology, Cardiovascular Research Institute Maastricht, Universiteit Maastricht, Maastricht, the Netherlands

The short-term (<24 h) consequences of oxidative stress induced by ischaemia–reperfusion (IR) have been studied extensively in the mouse heart. However, much less is known about the long-term effects inflicted by a brief ischaemic period on the murine heart. We therefore examined the structural and functional consequences of a 30 min ischaemic period after 2 and 8 weeks of reperfusion and compared these to the effects induced by permanent occlusion of the left anterior descending coronary artery (LAD). The latter procedure resulted in transmural myocardial infarcts of about 52% of the left ventricle. In contrast, the single 30 min ischaemic period led to infarct sizes of about 13% of the left ventricle (range, 4–23%) at 2 and 8 weeks after reperfusion. Maximal cardiac contractility responses (+dP/dt) to dobutamine infusion and volume loading were depressed at 2, but not at 8 weeks after IR. The restoration of cardiac contractility at 8 weeks after IR was associated with a significant 20% enlargement of the end-diastolic volume and 16% increase of the left ventricular wall thickness. These changes in cardiac geometry were less pronounced at 2 weeks after IR. Histological examination revealed that the IR injury was associated with prominent calcification. At 2 and at 8 weeks after IR, 25 ± 5 and 38 ± 5% of the injured area was calcified as observed in 69 and 73% of the animals, respectively. After permanent occlusion of the LAD, calcification was not observed and healing of the affected area was characterized by thinning and dilatation of the infarcted myocardium. These data indicate that, in mice, a single 30 min period of ischaemia reduced ventricular contractility up to at least 2 weeks after reperfusion. However, 8 weeks after IR, cardiac function was restored by eccentric hypertrophy associated with calcification of the injured ventricular wall.

(Received 11 March 2004; accepted after revision 29 June 2004; first published online 15 July 2004)
Corresponding author T. De Celle: Department of Pharmacology & Toxicology, Cardiovascular Research Institute Maastricht, Universiteit Maastricht, Maastricht, the Netherlands. Email: t.decelle{at}farmaco.unimaas.nl

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