{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,24]],"date-time":"2026-10-24T15:33:13Z","timestamp":1792855993475,"version":"4.5.0"},"reference-count":37,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"8","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation Research"],"published-print":{"date-parts":[[2018,4,13]]},"abstract":"<jats:sec>\n            <jats:title>\n              <jats:underline>Rationale:<\/jats:underline>\n            <\/jats:title>\n            <jats:p>Reduction of infarct size by remote ischemic perconditioning (perRIC) is evident only after several hours reperfusion.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>\n              <jats:underline>Objective:<\/jats:underline>\n            <\/jats:title>\n            <jats:p>To develop a potential real-time estimate of cardioprotection by perRIC, we have analyzed the time course of ST-segment elevation.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>\n              <jats:underline>Methods and Results:<\/jats:underline>\n            <\/jats:title>\n            <jats:p>\n              Anesthetized open-chest pigs were subjected to 60-minute coronary occlusion and 180-minute reperfusion (placebo; n=19). PerRIC (n=18; 4\u00d75 min\/5 min hindlimb occlusion\/reperfusion) was induced 20 minutes after coronary occlusion. Regional myocardial blood flow was measured with microspheres, areas of no-reflow with thioflavin-S, area at risk with blue dye, and infarct size with triphenyl tetrazolium chloride staining. Phosphorylation of protein kinase B \u03b1\/\u03b2\/\u03b3, extracellular signal-regulated kinase 1\/2, and signal transducer and activator of transcription 3 was determined by Western blot. ST-segment elevation was analyzed in a V2-like ECG-lead at baseline, 5- and 55-minute coronary occlusion, and 10-, 30-, 60-, and 120-minute reperfusion. Transmural blood flow at 5-minute coronary occlusion was not different between perRIC (0.029\u00b10.015 mL\/min per gram; mean\u00b1SD) and placebo (0.024\u00b10.018 mL\/min per gram) as was area at risk (perRIC: 24\u00b16% of the left ventricle; placebo: 21\u00b14%). Areas of no-reflow tended to be smaller with perRIC (9\u00b112% of area at risk versus 15\u00b114% with placebo;\n              <jats:italic>P<\/jats:italic>\n              =0.13). Infarct size with perRIC was 23\u00b112% of area at risk versus 40\u00b111% with placebo (\n              <jats:italic>P<\/jats:italic>\n              &lt;0.001). PerRIC increased phosphorylation of signal transducer and activator of transcription 3 at 120-minute reperfusion by 196\u00b1142% versus 109\u00b1120% with placebo (\n              <jats:italic>P<\/jats:italic>\n              =0.047). The time courses of ST-segment elevation in perRIC and placebo protocols, respectively, were different (\n              <jats:italic>P<\/jats:italic>\n              =0.017). With similar ST-segment elevation at 5-minute coronary occlusion (perRIC 282\u00b134 \u00b5V; placebo 259\u00b128 \u00b5V), partial recovery of ST-segment elevation between 5- and 55-minute coronary occlusion was more pronounced with perRIC than placebo (by 111\u00b184 versus 15\u00b194 \u00b5V;\n              <jats:italic>P<\/jats:italic>\n              =0.028).\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>\n              <jats:underline>Conclusion:<\/jats:underline>\n            <\/jats:title>\n            <jats:p>Infarct size reduction by perRIC is reflected in the ST-segment elevation during coronary occlusion in pigs, supporting the notion of protection from ischemic injury.<\/jats:p>\n          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Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andreas","family":"Skyschally","sequence":"additional","affiliation":[{"name":"From the Institute for Pathophysiology, West German Heart and Vascular Center, University of Essen Medical School, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gerd","family":"Heusch","sequence":"additional","affiliation":[{"name":"From the Institute for Pathophysiology, West German Heart and Vascular Center, University of Essen Medical School, 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