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Am J Physiol Heart Circ Physiol 288: H2588-H2593, 2005. First published January 21, 2005; doi:10.1152/ajpheart.01060.2004
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Impaired resting perfusion in viable myocardium distal to chronic coronary stenosis in rats

Christiane Waller,1 Tobias Engelhorn,3 Karl-Heinz Hiller,2 Gerd Heusch,4 Georg Ertl,1 Wolfgang Rudolf Bauer,1 and Rainer Schulz4

1Medizinische Universitätsklinik and 2Physikalisches Institut, Würzburg; and 3Abteilung für Neuroradiologie and 4Institut für Pathophysiologie, Universität Essen, Essen, Germany

Submitted 15 October 2004 ; accepted in final form 13 December 2004

Chronic coronary artery stenosis results in patchy necrosis in the dependent myocardium and impairs global and regional left ventricular (LV) function in rats in vivo. The aim of the present study was to compare regional myocardial blood flow (RMBF) and function (F) in poststenotic myocardium by using magnetic resonance imaging (MRI) and to compare MRI blood flow changes to histological alterations to assess whether RMBF in the viable poststenotic tissue remains normal. MRI was performed in 11 anesthetized Wistar rats with 2-wk stenosis of the left coronary artery. Postmortem, the extent of fibrotic tissue was quantified. Poststenotic RMBF was significantly reduced to 2.21 ± 0.30 ml·g–1·min–1 compared with RMBF in the remote myocardium (4.05 ± 0.50 ml·g–1·min–1). A significant relationship between the poststenotic RMBF (%remote area) and the poststenotic F (%remote myocardium) was calculated (r = 0.61, P < 0.05). Assuming perfusion in scar tissue to be 32 ± 5% of perfusion of remote myocardium, as measured in five additional rats, and that in remote myocardium to be 114 ± 25% of that in normal myocardium, as assessed in five sham rats, the calculated perfusion in partially fibrotic tissue samples (35.7 ± 5.2% of analyzed area) was 2.88 ± 0.18 ml·g–1·min–1, whereas measured MRI perfusion was only 1.86 ± 0.24 ml·g–1·min–1 (P < 0.05). These results indicate that resting perfusion in viable poststenotic myocardium is moderately reduced. Alterations in global and regional LV function are therefore secondary to both patchy fibrosis and reduced resting perfusion.

ischemic cardiomyopathy; necrosis



Address for reprint requests and other correspondence: C. Waller, Universitätsklinik Würzburg, Medizinische Klinik, Josef-Schneider-Strasse 2, 97080 Würzburg, Germany (E-mail: waller_c{at}medizin.uni-wuerzburg.de)




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