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dc.contributor.authorArslan, Mustafa
dc.contributor.authorPoyraz, Fatih
dc.contributor.authorKiraz, Hasan Ali
dc.contributor.authorAlkan, Metin
dc.contributor.authorKip, Gulay
dc.contributor.authorErdem, Ozlem
dc.contributor.authorComu, Faruk Metin
dc.date.accessioned2020-06-25T18:12:38Z
dc.date.available2020-06-25T18:12:38Z
dc.date.issued2015
dc.identifier.issn1607-8322
dc.identifier.issn2220-5799
dc.identifier.urihttps://hdl.handle.net/20.500.12587/5992
dc.descriptionErdem, Ayhan/0000-0001-7761-1078; Arslan, Mustafa/0000-0003-4882-5063;en_US
dc.descriptionWOS: 000421768300004en_US
dc.description.abstractObjective: Ischemia/reperfusion (I/R) injury is an important cause of myocardial damage by means of oxidative, inflammatory, and apoptotic mechanisms. The aim of the present study was to examine the potential cardio-protective effects of dexmedetomidine in a diabetic rat model of myocardial I/R injury. Methodology: A total of 18 streptozotocin (55 mg/kg) induced diabetic Wistar Albino rats were randomly divided into three equal groups as follows: the diabetic I/R group (DIR) in which myocardial I/R was induced by ligating the left anterior descending (LAD) coronary artery for 30 min, followed by 2 hours of reperfusion following left thoracotomy, the diabetic I/R dexmedetomidine group (DIRD) which were given 100 mu g/kg dexmedetomidine intraperitoneally 30 min before I/R induction by the same method and the diabetic control group (DC) which underwent sham operations without tightening of the coronary sutures. As a control group (C), 6 healthy age-matched Wistar Albino rats underwent sham operations similar to DC group. After the operation the rats were sacrificied and the myocardial tissues were histopathologically examined. Results: Microscopic myonecrosis findings were significantly different among groups (p= 0.008). Myonecrosis findings were significantly higher in DIR compared to C, DC and DIRD groups (p= 0.001, p=0.007 and p=0.037 respectively). Similarly microscopic inflammatory cell infiltration degrees showed significant differences among groups (p<0.0001). Compared to C, DC and DIRD groups, the microscopic inflammatory cell infiltration was significantly higher among DIR group (p<0.0001, p<0.0001 and p=0.009 respectively). Also myocardial tissue edema was significantly different among groups (p=0.002). The microscopic myocardial tissue edema levels were significantly higher in DIR group than C and DIRD groups (p<0.0001 and p=0.022 respectively). Tissue edema was also more prominent in DC compared to C group (p=0.022) Conclusion: Taken together our data indicate that dexmedetomidine may be helpful in reducing myocardial necrosis, myocardial inflammation and myocardial tissue edema resulting from ischemia/reperfusion injury.en_US
dc.language.isoengen_US
dc.publisherAnaesthesia Pain & Intensive Careen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectIschemia reperfusionen_US
dc.subjectDexmedetomidineen_US
dc.subjectMyonecrosisen_US
dc.subjectInflammatory cell infiltrationen_US
dc.subjectDiabetic raten_US
dc.titleThe effect of dexmedetomidine on myocardial ischemia reperfusion injury in streptozotocin induced diabetic ratsen_US
dc.typearticleen_US
dc.contributor.departmentKırıkkale Üniversitesien_US
dc.identifier.volume19en_US
dc.identifier.issue4en_US
dc.identifier.startpage444en_US
dc.identifier.endpage451en_US
dc.relation.journalAnaesthesia Pain & Intensive Careen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US


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