The Relationship Of Dexmedetomidine With Biochemical Parameters And Intraparenchymal Pressure

Introduction: In this study, in order to shed light on the intraparenchymal pressure reduction mechanism of dexmedetomidine, the effect of two different doses of 80 and 320 µg kg-1 on the levels of vasoconstrictor Endothelin-1(ET-1) and vasodilator prostaglandin I2 (PGI2) in blood and cerebrospinal fluid (CSF) in transient global cerebral ischemia model in rabbits was examined. This study was conducted in the Selcuk University Experimental Medicine Research Center between June 2005 and January 2006 and approved by an ethical committee. All rabbits were randomly divided into four groups; six rabbits in each group. In Group 1, a craniotomy was performed and the ischemia was not created. In Group 2, only an ischemia-reperfusion was performed. During reperfusion, 80 µg kg-1 intravenous dexmedetomidine was administered to Group 3, and 320 µg kg -1 intravenous dexmedetomidine was administered to Group 4. After the application of craniotomy and cervical neck dissection of the rabbits in Groups 2, 3 and 4, the bilateral carotid arteries were clamped and an ischemia was performed for one hour. Then, the clamps were removed and reperfusion was performed for one hour. In addition, ıntraparenchymal pressure were recorded after craniotomy and reperfusion. Blood and CSF samples were collected from rabbits after craniotomy in Group 1 and reperfusion in Groups 2,3 and 4 to determine levels of ET-1 and PGI2. Intraparenchymal pressure values after the reperfusion in Group II and IV were significantly higher than Group I( p< 0.05), but any significant increase in Group III (p>0.05). ET-1 levels of both blood and CSF were increased in the group performed ischemia and reperfusion and no treatment (Group II) and the group administered low dose dexmedetomidine (Group III) were similar with the sham group (p>0.05). However, PGI2 levels of CSF were significantly decreased in the group administered low dose dexmedetomidine (p< 0.05). Dexmedetomidine can reduce the intraparenchymal pressure by reducing the level of ET-1 in the transient global cerebral ischemia model.