{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,9]],"date-time":"2026-09-09T12:27:03Z","timestamp":1788956823871,"version":"build-2803163510"},"reference-count":23,"publisher":"SAGE Publications","issue":"4","license":[{"start":{"date-parts":[[2014,8,28]],"date-time":"2014-08-28T00:00:00Z","timestamp":1409184000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["J Renin Angiotensin Aldosterone Syst"],"published-print":{"date-parts":[[2015,12]]},"abstract":"<jats:sec>\n                    <jats:title>Introduction:<\/jats:title>\n                    <jats:p>\n                      Pharmacological preconditioning limits myocardial infarct size after ischemia\/reperfusion. Dexmedetomidine is an \u03b1\n                      <jats:sub>2<\/jats:sub>\n                      -adrenergic receptor agonist used in anesthesia that may have cardioprotective properties against ischemia\/reperfusion injury. We investigated whether dexmedetomidine induces cardioprotection against myocardial apoptosis injury.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods:<\/jats:title>\n                    <jats:p>In order to assess the role of dexmedetomidine on myocardial apoptosis, we established a grave scalding rat model. Blood and myocardial tissue from the ventriculus sinister were harvested, then troponin, myocardial apoptosis, and expression of caspase-12, GRP78, and CHOP were assessed.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>Dexmedetomidine significantly reduced myocardial apoptosis, improved functional recovery, and reversed myocardial injury induced by grave scalding. The heart rate in the five groups studied was significantly different ( p &lt; 0.05). The number of buffy-stained nucleoli in the myocardial cell was highest in the simple scald group. The expression of caspase-12 obviously increased in the simple scald group. The expression of GRP78 and CHOP increased in the simple scald and scald and 50 \u03bcg\/kg dexmedetomidine groups ( p &lt; 0.05).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions:<\/jats:title>\n                    <jats:p>The results show that dexmedetomidine (DEX) produces cardioprotection against myocardial apoptosis injury. DEX is not only a useful sedative, but also plays a pivotal role in anesthetic cardioprotection. The potential benefits of DEX protection in high risk cardiovascular patients undergoing surgery are enormous.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1177\/1470320314546941","type":"journal-article","created":{"date-parts":[[2014,8,29]],"date-time":"2014-08-29T20:10:00Z","timestamp":1409343000000},"page":"1274-1280","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":8,"title":["The efficacy and mechanism of dexmedetomidine in myocardial apoptosis via the renin\u2013angiotensin\u2013aldosterone system"],"prefix":"10.1177","volume":"16","author":[{"given":"Huishu","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Anesthesiology, Zhujiang Hospital of Southern Medical University, China"},{"name":"Affiliated Union Hospital, Fujian Medical University, 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