before and after the treatment MRI analysis was performed. After treatment, animals were sacrificed and analyzed. EGFP-labeled stem cells were found in the myocardium of treated animals. Three of five treated MCP-1 mice showed a significant increase in the ejection fraction. The left atrium was of normal size, with reduced thrombus formation, inflammatory cell accumulations, and cardiomyocyte negative regions. In ven- tricles and atrium, collagen VI deposition was reduced and sho- wed an improvement of the fibers organization. The pattern of connexin 43 remained disorganized. In addition, MMP-1 and -9 levels were increased indicating ongoing collagen degradation. Our results indicate that injection of mesenchymal adult stem cells has an anti-inflammatory effect on the left atrium of MCP-1 mice and improves cardiac function thus counter-acting left atrial dilatation and extracellular matrix deposition but not electrical remodeling. doi:10.1016/j.yjmcc.2006.03.076 062. A novel method to correct the electrocardiogram QT interval for changes in heart rate Helen K. Graham, Andrew W. Trafford. Unit of Cardiac Physiology, University of Manchester, 3.08 Core Technology Facility, Manchester M13 9NT, UK Determining the electrocardiogram QT interval, a prognostic indicator of ventricular arrhythmias, is complicated by rate- dependent changes in ventricular action potential duration and hence QT interval. Several methods exist to correct QT interval (QT c ) for changes in rate. However, these methods e.g. Bazett’s lead to overcorrection or underestimation of QT interval at high and low heart rates respectively and are thus of limited use in disease or drug discovery settings with concomitant changes in heart rate. We have therefore sought to define a rate-independent method for correcting QT interval that is sensitive to maneuvers that alter QT interval e.g. heart disease. Heart failure was induced in adult male ferrets by aortic coarctation and the electrocardiogram recorded using telemetry. A waveform recognition algorithm (EMKA Technologies) was used to determine the RR and QT intervals which were then binned into 10 ms RR groups. The average QT interval (QT 300 ) at an RR of 300 ms (the resting heart rate) was calculated and a correction factor determined by dividing the average QT interval for each 10 ms RR bin by QT 300 resulting in an inverse second order correction function. The relationship between RR and QT intervals was abolished following correction (uncorrected r 2 = 0.48, corrected r 2 = 0.004, P < 0.001). Furthermore, in heart failure, QT interval increased by 26 ms (P < 0.001) yet was unaltered in sham animals. In summary we present a new method correcting QT interval independently of changes in heart rate that detects differences in QT interval in a disease setting. Acknowledgment Supported by The British Heart Foundation. doi:10.1016/j.yjmcc.2006.03.077 063. PPARA is involved in triiodothyronine-induced cardiac hypertrophy and high-energy phosphate metabolism: A 31 P MRS study of the PPARA-null mouse Wen Zhang, Michiel ten Hove, Stefan Neubauer, Kieran Clarke. University of Oxford, UK Triiodothyronine (T3) acts via nuclear receptors to cause cardiac hypertrophy and alter cardiac energy metabolism. Peroxisome proliferator-activated receptor al- pha (PPARa) is a nuclear receptor that plays an important role in cardiac fatty acid metabolism. Both the T3 receptor and PPARa form heterodimers with the retinoid  receptor (RXR), the heterodimers bind to T3 and peroxisome proliferator response elements, respective- ly, to stimulate the transcription of T3-responsive genes or genes involved in fatty acid metabolism. Here, we aimed to determine whether cross-talk occurs between the two nuclear receptors using T3 stimulation of PPARa-null mice. After 7 days T3 injection, mouse hearts were isolated and perfused in the Langendorff mode in an MR spectrometer. In non-T3-treated control and PPARa-null mice, heart weight was the same. Phosphocreatine (PCr) was 26% lower (P < 0.01) in PPARa-null mouse hearts, but ATP and Pi were the same as controls. T3 treatment resulted in a 36% (P < 0.01) increase in heart weight in control mice, but only a 22% (P < 0.05) increase in PPARa-null mice so heart weight was 16% lower (P < 0.05) in PPARa-null mice than controls. However, T3 treatment caused all hearts to lose 46% (P < 0.01) of their initial PCr and the difference of PCr was not significant between control and PPARa-null mouse hearts. In conclusion, PPARa activation is required to maintain normal cardiac PCr concentrations, but exacerbate the hypertrophy caused by T3 stimulation. Thus, interactions between T3 and PPARa nuclear receptors alter the cardiac phenotype. doi:10.1016/j.yjmcc.2006.03.078 064. Treatment with a 5-HT 4 serotonin receptor antagonist improves function of the failing heart J.A.K. Birkeland a,c , I. Sjaastad a,c,d , T. Brattelid b,c , E. Qvigstad b,c , E.R. Moberg b,c , K.A. Krobert b,c , R. Bjørnerheim d , T. Skomedal b,c , O.M. Sejersted a,c , J.-B. Osnes b,c , F.O. Levy b,c . a Inst. for Exp. Med. Res., Norway. b Department of Pharmacology, Norway. c Center for Heart Failure Res., Univ. of Oslo, Norway. d Department of Cardiology, Ullevaal Univ. Hosp., Oslo, Norway Serotonergic inotropic response is induced in the left ventricle (LV) in rats with congestive heart failure (CHF) associated with upregulation of the G s -coupled 5-HT 4 receptor. Blockade of G s -coupled h-adrenoceptors is beneficial in CHF. We investigated whether treatment with ABSTRACTS / Journal of Molecular and Cellular Cardiology 40 (2006) 920 – 1015 943