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We studied the fluxes of a potassium congener (Rb(+)) in mouse hearts by (87)Rb MRS at 8.4T. The hearts were loaded with Rb(+) by perfusion with Krebs-Henseleit buffer, in which 50% of K(+) was substituted with Rb(+). We initiated Rb(+) efflux by changing the perfusion medium to Rb(+)-free buffer. Spectra were acquired every 1.85 min, and the kinetics of Rb(+) transport were analyzed by means of monoexponential fits. The rate constants of Rb(+) uptake and efflux were 0.0680 +/- 0.0028 and 0.0510 +/- 0.0051 min(-1), respectively (approximately 30% faster than in the rat heart). The ATP-sensitive potassium channel opener, P-1075 (5 microM), and mitochondrial uncoupler, 2,4-dintrophenol (50 microM), activated Rb(+) efflux from mouse hearts by approximately 35%. The mechanisms responsible for the differences in Rb(+) uptake and efflux under baseline conditions and stimulation, in comparison with rat hearts, are discussed. These data provide a background for studies of cardiac potassium transport in transgenic mouse strains., (Copyright 2005 Wiley-Liss, Inc.)

87Rb-MRI was used to measure Rb(+) uptake in blood-perfused pig hearts during complete occlusion (120 and 70 min) of the left anterior descending artery (LAD) and subsequent reperfusion (120 and 170 min). The Rb(+) uptake rate and maximal Rb image intensity during 120-min occlusion were significantly lower in the ischemic anterior left ventricular (LV) wall (0.35 +/- 0.14%/min and 26 +/- 4.7%) relative to those in the remote posterior LV wall (2.43 +/- 0.33%/min and 98 +/- 10%). Reperfusion after 120 and 70 min of occlusion resulted in formation of damaged areas, which had 40 +/- 4 and 73 +/- 10% of the (87)Rb image intensity observed in the remote posterior wall. The infarct sizes determined histologically by triphenyltetrazolium chloride staining were 9.6 +/- 3.4 and 5.6 +/- 4.6% of the total ventricular mass (LV + RV) in the 120- and 70-min occlusion groups, respectively. The sizes determined by MRI were 13.1 +/- 2 and 2.8 +/- 4.3% of the total number of pixels, respectively. The Rb(+) uptake in the anterior wall during 120-min occlusion was somewhat lower than that previously observed in crystalloid-perfused hearts. It is concluded that blood does not interfere with the ability of (87)Rb MRI to detect ischemic and infarct areas., (Copyright 2003 Wiley-Liss, Inc.)

The cardioprotective properties of inhibition of poly (ADP-ribose) synthetase (PARS) were investigated in the isolated perfused heart of the rat. Hearts were perfused in the Langendorff mode and subjected to 23 min total global ischaemia and reperfused for 60 min. Left ventricular function was assessed by means of an intra-ventricular balloon. High energy phosphates were measured by 31P-NMR spectroscopy. Intracellular levels of NAD were measured by capillary electrophoresis of perchloric acid extracts of hearts at the end of reperfusion. Reperfusion in the presence of the PARS inhibitor 1,5 didroxyisoquinoline (ISO, 100 microM) attenuated the mechanical dysfunction observed following 1 h of reperfusion; 27+/-13 and 65+/-8% recovery of preischaemic rate pressure product for control and 100 microM ISO, respectively. This cardioprotection was accompanied by a preservation of intracellular high-energy phosphates during reperfusion; 38+/-2 vs 58+/-4% (P<0.05) of preischaemic levels of phosphocreatine (PCr) for control and 100 microM ISO respectively and 23+/-1 vs 31+/-3% (P < 0.05) of preischaemic levels of ATP for control and 100 microM ISO respectively. Cellular levels of NAD were higher in ISO treated hearts at the end of reperfusion; 2.56+/-0.45 vs 4.76+/-1.12 micromoles g(-1) dry weight (P<0.05) for control and ISO treated. These results demonstrate that the cardioprotection afforded by inhibition of PARS activity with ISO is accompanied by a preservation of high-energy phosphates and cellular NAD levels and suggest that the mechanism responsible for this cardioprotection may involve prevention of intracellular ATP depletion.

The aim of this work was to investigate whether 1) Rb uptake is reduced in ischemic myocardium, and 2) 87Rb three-dimensional (3D) imaging can detect the ischemic area. Hearts of domestic pigs (n = 8, 20-30 kg) were perfused retrogradely with Krebs-Henseleit buffer in a 7-T, 40-cm horizontal bore magnet interfaced with Bruker MSLX spectrometer. Control (C) and ischemic (I) (45 min ligation of the left anterior descending coronary artery (LAD)) hearts were loaded with Rb+ by perfusion with a Rb(+)-containing solution (2-4.7 mM, 30-100% of K+ substitution) for 35 min and 87Rb (C) or 31P (ischemic area in I) spectra were acquired. After mechanical arrest with 0.6-0.9 mM lidocaine, 87Rb images (7 min each, 1 cm3 resolution) were acquired (30-40 min) in the presence of Rb(+)-containing perfusate. Subsequently, the hearts were stained with Evans blue (EB) and samples taken for measurements of Rb+ content. In the Group C, distribution of Rb+ in the left ventricle and the intensities of the 3D 87Rb images were uniform. In the ischemic area (Group I), verified by the lack of EB staining and changes in 31P spectra, the images showed a reduced intensity, which corresponded to decreased Rb+ content (33 +/- 11% of the normal). Thus, 87Rb imaging reveals damaged cells detecting reduced Rb+ content in the ischemic area.