Eksperimental global serebral iskemi modelinde deksmedetomidinin kafa içi basınç ve lipid peroksidasyonuna etkileri
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Tarih
2006
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Selçuk Üniversitesi Tıp Fakültesi
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info:eu-repo/semantics/openAccess
Özet
Biz bu deneysel çalışmada serebral iskemi oluşturulan deneklere 80 µg/kg ve 320 µg/kg deksmedetomidin uygulayarak, bu ajanın hemodinamik parametrelere, intrakranial basınca ve doku MDA düzeylerine etkilerini inceleyerek yararlılığını tespit etmeyi amaçladık. Çalışmamızda kiloları 3000-3500 gram arasında değişen 24 adet Yeni Zellanda tipi tavşan kullanıldı. Tüm tavşanlara intramüsküler (i.m) 15 mg/kg xylazine HCL (Rompun %2 BAYER) ve 35 mg/kg ketamine HCL (ketalar PARKE-DAVIS, Eczacıbaşı) ile anestezi verildi. Bütün denekler çalışma süresince spontan solunumda muhafaza edildi. Deneklere servikal boyun diseksiyonu yapılarak bilateral karotis arter klemplenerek bir saat boyunca iskemi ve daha sonrasında klempler açılarak bir saat reperfüzyon uygulandı.Her grupta 6 tavşan olacak şekilde rastgele 4 gruba ayrılan deneklerden I. gruba iskemi oluşturulmazken, II. gruba iskemi reperfüzyon uygulanarak tedavi verilmemiş, III. gruba reperfüzyon sırasında 80 µg/kg deksmedetomidin, IV. gruba reperfüzyon sırasında 320 µg/kg deksmedetomidin ilk 10 dakika içerisinde ıv olarak uygulandı.Bütün grupların sistolik (SAB), diyastolik (DAB), ortalama (OAB) arter basınçları, kalp atım hızları (KAH); ; kraniotomiden önce (bazal), kraniotomiden sonra, iskemi sonrası (60.dk) ve reperfüzyon sonrası (120.dk) olarak kaydedildi. İntraparankimal ısı ve intraparankimal basınç değerleri kraniotomiden sonra, iskemi sonrası (60.dk) ve reperfüzyon sonrası (120.dk) olarak kaydedildi. Reperfüzyon sonrasında deneklerden 1 gram beyin dokusu alındı, canlılığını sürdüren denekler ise yüksek doz pentotal ile sakrifiye edildi. SAB, DAB, OAB ve KAH bütün gruplarda kraniotomi sonrası artmış olup iskemi sonrasında (60.dk) azalmıştır. Reperfüzyon sonrası (120.dk) değerleri deksmedetomidinin sırasıyla 80 ve 320 µg/kg uygulandığı Grup 3 ve Grup 4 de anlamlı olarak azalmıştır (p<0.05). İntraparankimal basınç, bütün gruplarda iskemi sonrasında (60.dk)) artmış olmasına rağmen gruplar arası ve grup içi değerlendirmelerinde anlamlı farka rastlanmadı (p>0.05). Reperfüzyon sonrası dönemde ise sham grubuna (Grup 1) göre intraparankimal basınç diğer gruplarda anlamlı olarak daha yüksek tespit edildi (p<0.05). 320 µg/kg deksmedetomidin uygulanan grupta intraparankimal basınç daha az yükselme gösterirken, 80 µg/kg 55 deksmedetomidin uygulanan grupla arasında anlamlı bir farka rastlanamadı (p >0.05), bu iki gruba göre kontrol grubunda (Grup 2) intraparankimal basınç daha yüksek saptandı (p<0.05). Çalışma süresince intaparankimal olarak ölçülen serebral ısı tüm gruplarda 36ºC'nin altına düşmedi ve stabil seyretti. Gruplar arasında, çalışma süresince kaydedilen periyotlarda anlamlı fark tespit edilmedi (p>0.05). Tüm gruplarda MDA değerleri sham grubu (Grup1) ile karşılaştırıldığında; kontrol (Grup 2) ve düşük doz deksmedetomidin uygulanan grupta (Grup 3) daha yüksek MDA düzeyleri elde edilirken (p<0.05), yüksek doz deksmedetomidin uygulanan grup (Grup 4) ile sham grubu arasında anlamlı fark tespit edilemedi (p>0.05). Fakat yüksek doz deksmedetomidin uygulanan grubun (Grup 4) MDA düzeyleri kontrol ve düşük doz deksmedetomidin grubuna göre daha düşük olmasına rağmen bu iki grup (Grup 2 ve 3) ile aralarında istatistiksel açıdan anlamlı fark yoktu. Sonuç olarak çalışmamız; global serebral iskemi olgularında deksmedetomidin kullanıldığında intraparankimal basınç artışını azalttığını ve bunda doz artırımının anlamlı bir fark sağlamadığını, ayrıca iskemi reperfüzyon hasarında meydana gelen lipid peroksidasyon son ürünü olan MDA'yı azaltarak serebral korumada etkin olabileceğini göstermiştir.
In this experimental study, we aimed to evaluate the effects of dexmedetomidinine on intraparanchymal pressure and lipid peroxidation by administering 80 µg/kg and 320 µg/kg dexmedetomidinine to samples that were prepared for cerebral ischemia. In our study; 24 New Zeland type rabbits weighed between 3000-3500 grams were used. All rabbits were anesthesized by intramuscular (ım) 15 mg/kg xylazine HCL (Rompun %2 BAYER) and 35 mg/kg ketamine HCL (ketalar PARKE-DAVIS, Eczacıbaşı).All samples were kept in spontaneus respiration during study period. Cervical neck dissection was applied to all samles and cerebral ischemia was created by clomping bilateral carotid arteries for 1 hour and then reperfucion was supplied for 1 hour by disclosure of the clamps. All samples were grouped randomly in 4 groups; supplying 6 rabbits in each group. In the first group ischemia was not created, in the 2. group ischemia reperfusion was applied and not treated, in the 3. group during reperfusion 80 µg/kg dexmedetomidine and the 4. group during reperfusion 320 µg/kg dexmedetomidine was administered within first 10 minutes introvenously.Systolic (SAP), diastolic (DAP), and the mean arterial pressure (MAP), heart rates (HR) of all groups were recorded before craniotomy (bazal); after craniotomy, during ischemia (60.min) and after reperfusion (120.min). After reperfusion 1 gr of brain tissue was collected from samples were sacrified by high dose penthotal. SAP, DAP, MAP and HR were all found to be increased after craniotomy in all groups; whereas after ischemia (60.min) all decreased to normal levels before cranitomy. Values after reperfusion (120.min) was found to be significantly decreased in group 3 and 4 in which 80 µg/kg and 320 µg/kg dexmedetomidine was administered respectively (p<0.05). Intraparanchymal pressure was observed to be increased after ischemia (60.min) in all groups, but the interpretation of results among groups was not statistically significant (p>0.05). After reperfucion period; intraparanchymal pressure was found to be significantly higher in groups other than sham group (group 1) (p<0.05). In 320 µg/kg dexmedetomidine 57 administered group, the intraparanchymal pressure showed less increase; but when compared to group in which 80 µg/kg dexmedetomidine was administered; there was not any statisticaly significant difference (p>0.05); compared with these 2 groups; the intraparanchymal pressure was found to be higher in control group (group 2) (p<0.05). When MDA levels in all groups are compared with sham group (group 1); in control (group 2) and low dose dexmedetomidine administered group (group 3) higher MDA levels were obtaired (p<0.05); whereas there was no statistically significant difference between high dose dexmedetomidine administered group (group 4) (p<0.05). As a result, our study supports that when dexmedetomidine is used in global cerebral ischemia cases; it can diminsh increase in intraparanchymal pressure and increased doses don?t lead to significant differences by this aspect, besides it can also diminish the MDA levels that are the last product in lipid peroxidation during ischemia-reperfusion damage, and by this way it can be effective in brain protection.
In this experimental study, we aimed to evaluate the effects of dexmedetomidinine on intraparanchymal pressure and lipid peroxidation by administering 80 µg/kg and 320 µg/kg dexmedetomidinine to samples that were prepared for cerebral ischemia. In our study; 24 New Zeland type rabbits weighed between 3000-3500 grams were used. All rabbits were anesthesized by intramuscular (ım) 15 mg/kg xylazine HCL (Rompun %2 BAYER) and 35 mg/kg ketamine HCL (ketalar PARKE-DAVIS, Eczacıbaşı).All samples were kept in spontaneus respiration during study period. Cervical neck dissection was applied to all samles and cerebral ischemia was created by clomping bilateral carotid arteries for 1 hour and then reperfucion was supplied for 1 hour by disclosure of the clamps. All samples were grouped randomly in 4 groups; supplying 6 rabbits in each group. In the first group ischemia was not created, in the 2. group ischemia reperfusion was applied and not treated, in the 3. group during reperfusion 80 µg/kg dexmedetomidine and the 4. group during reperfusion 320 µg/kg dexmedetomidine was administered within first 10 minutes introvenously.Systolic (SAP), diastolic (DAP), and the mean arterial pressure (MAP), heart rates (HR) of all groups were recorded before craniotomy (bazal); after craniotomy, during ischemia (60.min) and after reperfusion (120.min). After reperfusion 1 gr of brain tissue was collected from samples were sacrified by high dose penthotal. SAP, DAP, MAP and HR were all found to be increased after craniotomy in all groups; whereas after ischemia (60.min) all decreased to normal levels before cranitomy. Values after reperfusion (120.min) was found to be significantly decreased in group 3 and 4 in which 80 µg/kg and 320 µg/kg dexmedetomidine was administered respectively (p<0.05). Intraparanchymal pressure was observed to be increased after ischemia (60.min) in all groups, but the interpretation of results among groups was not statistically significant (p>0.05). After reperfucion period; intraparanchymal pressure was found to be significantly higher in groups other than sham group (group 1) (p<0.05). In 320 µg/kg dexmedetomidine 57 administered group, the intraparanchymal pressure showed less increase; but when compared to group in which 80 µg/kg dexmedetomidine was administered; there was not any statisticaly significant difference (p>0.05); compared with these 2 groups; the intraparanchymal pressure was found to be higher in control group (group 2) (p<0.05). When MDA levels in all groups are compared with sham group (group 1); in control (group 2) and low dose dexmedetomidine administered group (group 3) higher MDA levels were obtaired (p<0.05); whereas there was no statistically significant difference between high dose dexmedetomidine administered group (group 4) (p<0.05). As a result, our study supports that when dexmedetomidine is used in global cerebral ischemia cases; it can diminsh increase in intraparanchymal pressure and increased doses don?t lead to significant differences by this aspect, besides it can also diminish the MDA levels that are the last product in lipid peroxidation during ischemia-reperfusion damage, and by this way it can be effective in brain protection.
Açıklama
Anahtar Kelimeler
Eksperimental global serebral iskemi, Experimental global cerebral ischemia, Deksmedetomid, Kafa içi basınç, Intracranial pressure, Lipid peroksidasyonu, Lipid peroxidation
Kaynak
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Scopus Q Değeri
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Sayı
Künye
Bardakçı, H. K. (2006). Eksperimental global serebral iskemi modelinde deksmedetomidinin kafa içi basınç ve lipid peroksidasyonuna etkileri. Selçuk Üniversitesi, Yayımlanmış uzmanlık tezi, Konya.
