{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,20]],"date-time":"2025-10-20T16:34:35Z","timestamp":1760978075369,"version":"build-2065373602"},"reference-count":37,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2002,8,1]],"date-time":"2002-08-01T00:00:00Z","timestamp":1028160000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["NMR in Biomedicine"],"published-print":{"date-parts":[[2002,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The effects of drugs that can modulate passive permeability of K<jats:sup>+<\/jats:sup> into cardiomyocytes in normal and reperfusion\u2010damaged cardiac muscle were assessed. Rubidium ion (Rb<jats:sup>+<\/jats:sup>) was used as a K<jats:sup>+<\/jats:sup> tracer and <jats:sup>87<\/jats:sup>Rb\u2010MRI as a detection method. The left anterior descending artery (LAD) of isolated pig hearts perfused with Krebs\u2013Henseleit buffer (KHB) was occluded for 2\u2005h and subsequently reperfused for 2\u2005h with KHB containing 4.7 m<jats:sc>M<\/jats:sc> RbCl instead of KCl. The buffer contained either a blocker of ATP\u2010sensitive K<jats:sup>+<\/jats:sup> channels (K<jats:sub>ATP<\/jats:sub>), glibenclamide (Glib, 3\u2005\u00b5<jats:sc>M<\/jats:sc>), a K<jats:sub>ATP<\/jats:sub> opener, pinacidil (Pin, 10\u2005\u00b5<jats:sc>M<\/jats:sc>), a K<jats:sup>+<\/jats:sup>\/Na<jats:sup>+<\/jats:sup>\/2Cl<jats:sup>\u2212<\/jats:sup> co\u2010transporter inhibitor, bumetanide (Bum, 10\u2005\u00b5<jats:sc>M<\/jats:sc>) or no drug (control). Upon reperfusion three\u2010dimensional <jats:sup>87<\/jats:sup>Rb MR images were acquired to obtain kinetics of Rb<jats:sup>+<\/jats:sup> uptake and its distribution. Areas at risk (AAR) and areas of necrosis were determined by Evans Blue and triphenyl tetrazolium chloride staining, respectively. Rb<jats:sup>+<\/jats:sup> uptake kinetics in the remote posterior (Pos) wall were similar in all groups. The kinetics remained monoexponential in the affected anterior (Ant) wall and the uptake rates were 32, 36, 37 and 21% of that in the Pos wall in the control, Glib, Pin and Bum groups, respectively. Infarct sizes determined histologically as a percentage of total ventricular (left\u2005+\u2005right) mass (14\u201322%) corresponded to sizes of areas with 20\u201340% of maximal Rb image intensity [I(Rb)<jats:sub>max<\/jats:sub>, 15\u201322%], except for the Pin group (12.5 <jats:italic>vs<\/jats:italic> 21%). The sizes of areas with 20\u201350% of I(Rb)<jats:sub>max<\/jats:sub> (30\u201336%) closely correlated with those of AAR determined histologically (31\u201333%). Lactate dehydrogenase release did not differ in all groups. We conclude that: (1) reperfusion damage quickly inhibits Rb<jats:sup>+<\/jats:sup> uptake; (2) Rb<jats:sup>+<\/jats:sup> uptake in normal and reperfused tissue does not significantly depend on K<jats:sub>ATP<\/jats:sub> or the K<jats:sup>+<\/jats:sup>\/Na<jats:sup>+<\/jats:sup>\/2Cl<jats:sup>\u2212<\/jats:sup> cotransporter; (3) areas with 20\u201340% of maximal image intensity correspond to infarct areas. 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