{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T22:14:00Z","timestamp":1791497640294,"version":"4.3.4"},"reference-count":59,"publisher":"Canadian Science Publishing","issue":"8","license":[{"start":{"date-parts":[[2017,8,1]],"date-time":"2017-08-01T00:00:00Z","timestamp":1501545600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/www.nrcresearchpress.com\/page\/about\/CorporateTextAndDataMining"}],"content-domain":{"domain":["cdnsciencepub.com"],"crossmark-restriction":false},"short-container-title":["Can. J. Physiol. Pharmacol."],"published-print":{"date-parts":[[2017,8]]},"abstract":"<jats:p> Diabetes mellitus, besides having deleterious effects, induces cardiac adaptation that may reduce the heart\u2019s susceptibility to ischemia\u2013reperfusion (IR) injury. This study aimed to investigate whether changes in mitochondrial properties are involved in the mechanisms of increased resistance of the diabetic heart to IR. Adult male Wistar rats were made diabetic by a single dose of streptozotocin (65 mg\u00b7kg<jats:sup>\u20131<\/jats:sup>, i.p.), and on the day 8, Langendorff-perfused hearts were subjected to 30 min global ischemia and 40 min reperfusion. Baseline preischemic parameters in the diabetic hearts did not differ markedly from those in the nondiabetic controls, except for lower left ventricular developed pressure, higher mitochondrial membrane fluidity, and protein levels of manganese superoxide dismutase. On the other hand, diabetic hearts showed significantly better post-IR functional restoration and reduced arrhythmogenesis associated with lower reactive oxygen species production as compared with healthy controls. IR decreased membrane fluidity in both experimental groups; however, it led to a complete recovery of mitochondrial Mg<jats:sup>2+<\/jats:sup>-ATPase activity in diabetics in contrast to its reduction in nondiabetics. These findings indicate that the heart may become adapted to diabetes-induced alterations that might increase its tolerance to an ischemic insult. Preserved mitochondrial function might play a role in the mechanisms of the heart\u2019s resistance to IR injury in diabetics. <\/jats:p>","DOI":"10.1139\/cjpp-2017-0211","type":"journal-article","created":{"date-parts":[[2017,7,6]],"date-time":"2017-07-06T21:35:03Z","timestamp":1499376903000},"page":"969-976","update-policy":"https:\/\/doi.org\/10.1139\/csp-crossmark-policy","source":"Crossref","is-referenced-by-count":7,"title":["Changes in mitochondrial properties may contribute to enhanced resistance to ischemia\u2013reperfusion injury in the diabetic rat heart"],"prefix":"10.1139","volume":"95","author":[{"given":"Martina","family":"Mur\u00e1rikov\u00e1","sequence":"first","affiliation":[{"name":"Institute for Heart Research, Slovak Academy of Sciences, Bratislava, Slovak Republic."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Miroslav","family":"Ferko","sequence":"additional","affiliation":[{"name":"Institute for Heart Research, Slovak Academy of Sciences, Bratislava, Slovak Republic."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Iveta","family":"Waczul\u00edkov\u00e1","sequence":"additional","affiliation":[{"name":"Division of Biomedical Physics, Department of Nuclear Physics and Biophysics, Faculty of Mathematics, Physics and Informatics, Comenius University, Bratislava, Slovak Republic."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Magdal\u00e9na","family":"Ja\u0161ov\u00e1","sequence":"additional","affiliation":[{"name":"Institute for Heart Research, Slovak Academy of Sciences, Bratislava, Slovak Republic."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ivana","family":"Kancirov\u00e1","sequence":"additional","affiliation":[{"name":"Institute for Heart Research, Slovak Academy of Sciences, Bratislava, Slovak Republic."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jana","family":"Mur\u00ednov\u00e1","sequence":"additional","affiliation":[{"name":"Institute of Normal and Pathological Physiology, Slovak Academy of Sciences, Bratislava, Slovak Republic."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"T\u00e1\u0148a","family":"Ravingerov\u00e1","sequence":"additional","affiliation":[{"name":"Institute for Heart Research, Slovak Academy of Sciences, Bratislava, Slovak Republic."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"155","reference":[{"key":"refg1\/ref1","doi-asserted-by":"publisher","DOI":"10.1016\/j.ahj.2007.06.020"},{"key":"refg2\/ref2","doi-asserted-by":"publisher","DOI":"10.1007\/s00125-005-0091-5"},{"key":"refg3\/ref3","doi-asserted-by":"publisher","DOI":"10.1007\/s13105-016-0530-4"},{"key":"refg4\/ref4","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.0000069215.36389.8D"},{"key":"refg5\/ref5","doi-asserted-by":"publisher","DOI":"10.1016\/j.cellsig.2011.09.007"},{"issue":"8","key":"refg6\/ref6","first-page":"23","volume":"55","author":"Brucknerov\u00e1 I.","year":"2000","journal-title":"Biologia"},{"issue":"2","key":"refg7\/ref7","first-page":"65","volume":"27","author":"Brucknerov\u00e1 I.","year":"2006","journal-title":"Neuroendocrinol. 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