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Received July 13, 2001
Accepted after revision September 28, 2001
1 Herchel Smith Laboratory for Medicinal Chemistry, University of Cambridge School of Clinical Medicine, Forvie Site, Robinson Way, Cambridge CB2 2PZ and Physiological Laboratory, Department of Physiology, University of Cambridge, Downing Site, Downing Street, Cambridge CB2 3EG, UK
2 Herchel Smith Laboratory for Medicinal Chemistry, University of Cambridge School of Clinical Medicine, Forvie Site, Robinson Way, Cambridge CB2 2PZ and Oxford Centre for Functional Magnetic Resonance Imaging of the Brain, University of Oxford, John Radcliffe Hospital, Headington, Oxford OX3 9DU, UK
3 Herchel Smith Laboratory for Medicinal Chemistry, University of Cambridge School of Clinical Medicine, Forvie Site, Robinson Way, Cambridge CB2 2PZ, UK
4 Department of Surgery, Box 202, Level 9, Addenbrooke's Hospital, Cambridge CB2 2QQ, UK
5 The Wolfson Brain Imaging Centre, University of Cambridge, Box 65, Addenbrooke's Hospital, Cambridge CB2 2QQ, UK
6 Physiological Laboratory, Department of Physiology, University of Cambridge, Downing Site, Downing Street, Cambridge CB2 3EG, UK
* To whom correspondence should be addressed. E-mail: clh11{at}cus.cam.ac.uk.
A non-invasive cine magnetic resonance imaging (MRI) technique was developed to allow, for the first time, detection and characterization of chronic changes in myocardial tissue volume and the effects upon these of treatment by the angiotensin-converting enzyme (ACE) inhibitor captopril in streptozotocin (STZ)-diabetic male Wistar rats. Animals that had been made diabetic at the ages of 7, 10 and 13 weeks and a captopril-treated group of animals made diabetic at the age of 7 weeks were scanned. The findings were compared with the results from age-matched controls. All animal groups (n = 4 animals in each) were consistently scanned at 16 weeks. Left and right ventricular myocardial volumes were reconstructed from complete data sets of left and right ventricular transverse sections which covered systole and most of diastole using twelve equally incremented time points through the cardiac cycle. The calculated volumes remained consistent through all twelve time points of the cardiac cycle in all five experimental groups and agreed with the corresponding post-mortem determinations. These gave consistent myocardial densities whose values could additionally be corroborated by previous reports, confirming the validity of the quantitative MRI results and analysis. The myocardial volumes were conserved in animals whose diabetes was induced at 13 weeks but were significantly increased relative to body weight in animals made diabetic at 7 and 10 weeks. Captopril treatment, which was started immediately after induction of diabetes, prevented the development of this relative hypertrophy in both the left and right ventricles. We have thus introduced and validated quantitative MRI methods in a demonstration, for the first time, of chronic myocardial changes in both the right and left ventricles of STZ-diabetic rats and their prevention by the ACE inhibitor captopril.
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