The effect of aprotinin on brain ischemic-reperfusion injury after hemorrhagic shock in rats: An experimental study

Basit Öğe Kaydı
dc.contributor.authorEser, Cay
dc.contributor.authorKalkan, Erdal
dc.contributor.authorCosar, Murat
dc.contributor.authorBuyukbas, Sadik
dc.contributor.authorAvunduk, Mustafa Cihat
dc.contributor.authorAslan, Adem
dc.contributor.authorKocabas, Volkan
dc.date.accessioned2020-03-26T17:18:26Z
dc.date.available2020-03-26T17:18:26Z
dc.date.issued2007
dc.departmentSelçuk Üniversitesien_US
dc.description.abstractBackground. We aimed to demonstrate the positive effects of the serine protease inhibitor aprotinin on neural ischemia-reperfusion injury and apoptosis in a rat model. Methods: There were 18 rats divided into 3 groups: group A (sham, n = 6), group B (ischemia-reperfusion, n = 6), and group C (ischemia-reperfusion + aprotinin, n = 6). The systolic blood pressure of the group B and C rats was decreased to 40% to 50% of the normal level by taking blood from the femoral vein to develop hemorrhagic shock. The blood was retained and given to the remaining group B and C rats for reperfusion 20 minutes after the procedure. In group B, isotonic solution and, in group C, aprotinin was administered to the rats 5 minutes before reperfusion. After the rats were killed, the brain tissue samples were fixed for histopathologic examination. Brain tissue superoxide dismutase, malondialdehyde, and tissue myeloperoxidase level and apoptotic cell analyses were performed in all groups. Results: Superoxide dismutase level decreased from group A to group B and increased from group B to group C (p < 0.05). Malondialdehyde and myeloperoxidase levels and apoptotic cells increased from group A to group B and decreased from group B to group C (p < 0.05). Conclusions: The results suggest that the systemic use of aprotinin in ischemic neural tissue prevents reperfusion injury and also protects the morphologic, functional, and biochemical integrity of the neural tissue.en_US
dc.identifier.doi10.1097/01.5a.0000236054.42254.b7en_US
dc.identifier.endpage378en_US
dc.identifier.issn0022-5282en_US
dc.identifier.issn1529-8809en_US
dc.identifier.issue2en_US
dc.identifier.pmid17693839en_US
dc.identifier.scopusqualityN/Aen_US
dc.identifier.startpage373en_US
dc.identifier.urihttps://dx.doi.org/10.1097/01.5a.0000236054.42254.b7
dc.identifier.urihttps://hdl.handle.net/20.500.12395/21661
dc.identifier.volume63en_US
dc.identifier.wosWOS:000248735300024en_US
dc.identifier.wosqualityQ1en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherLIPPINCOTT WILLIAMS & WILKINSen_US
dc.relation.ispartofJOURNAL OF TRAUMA-INJURY INFECTION AND CRITICAL CAREen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.selcuk20240510_oaigen_US
dc.subjectaprotininen_US
dc.subjectbrain injuryen_US
dc.subjectexperimentalen_US
dc.subjecthemorrhagic shocken_US
dc.subjectischemiaen_US
dc.subjectreperfusionen_US
dc.titleThe effect of aprotinin on brain ischemic-reperfusion injury after hemorrhagic shock in rats: An experimental studyen_US
dc.typeArticleen_US

Dosyalar

Koleksiyon

WoS İndeksli Yayınlar Koleksiyonu
PubMed İndeksli Yayın Koleksiyonu
Scopus İndeksli Yayınlar Koleksiyonu