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    Attenuation of vasospasm by demedetomidine after experimental subarachnoidal haemorrhage in rabbits
    (Tubitak Scientific & Technological Research Council Turkey, 2008) Eser, Olcay; Fidan, Hueseyin; Coskun, Oemer; Ela, Yueksel; Songur, Ahmet; Cosar, Murat
    Aim: Vasospasm is one of the most important factors that influence the successful treatment of ruptured intracranial aneurysm. We studied if vasospasm following subarachnoidal haemorrhage (SAH) can be alleviated by dexmedetomidine in an animal model. Materials and Methods: Experimental SAH was induced in 12 of 18 New Zealand rabbits by intracisternal injection of autologous blood. Control animals (sham SAH, n = 6) received intracisternal injection of the respective volume of physiological saline solution. Forty eight hours after the operation, rabbits in sham SAH and SAH-alone (n = 6) groups were infused intravenously with 0.9% sodium chloride for 2 h, whereas rabbits in SAH-dexmedetomidine group (n = 6) received intravenous infusion of 5 mu g/kg per In dexmedetomidine for 2 h. All rabbits were sacrificed with penthotal 24 h alter infusions. Basilar arteries were isolated and processed for histology. Results: The histological specimens revealed evidence of arterial narrowing and vascular wall thickening in both SAH-alone and SAH-dexmedetomidine groups. The wall thickness of basilar artery significantly increased and lumen diameter significantly reduced in SAH-alone group in comparison with basilar arteries from other groups (P < 0.05). SAH-dexmedetomidine group revealed attenuation of vasospasm formed after 72 h. Conclusions: Our study showed that vasospasm is attenuated by dexmedetomidine administered after vasospasm is formed in a rabbit model.
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    The neuroprotective effect of Sulindac after ischemia-reperfusion injury in rats1
    (Acta Cirurgica Brasileira, 2014) Cosar, Murat; Kaner, Tuncay; Sahin, Onder; Topaloglu, Naci; Guven, Mustafa; Aras, Adem Bozkurt; Akman, Tarik
    PURPOSE:To investigate the neuroprotective effects of Sulindac on the hippocampal complex after global cerebral ischemia/reperfusion (I/R) injury in rats. METHODS: Thirty one Sprague- Dawley rats were used, distributed into group I (sham) n: 7 were used as control. For group II (n: 8), III (n: 8) and IV (n: 8) rats, cerebral ischemia was performed via the occlusion of bilateral internal carotid artery for 45 minutes and continued with reperfusion process. 0.3 mL/kg/h 0.9 % sodium chloride was infused intraperitoneally to the Group II rats before ischemia, 5 mu g/kg/h/0.3 ml sulindac was infused intraperitoneally to the Group III rats before ischemia and 5 mu g/kg/h/0.3 ml sulindac was infused intraperitoneally to the Group IV rats after ischemia and before reperfusion process. The levels of MDA, GSH and MPO activity were measured in the left hippocampus tissue. The hippocampal tissue of all group members were taken for histopathological study. RESULTS: The MDA and MPO levels increased from group I (control) to group II (I/R) (P < 0.05) and decreased from group II (I/R) to group III (presulindac + I/R) and IV (postsulindac + I/R) (P < 0.05). Beside these, the GSH levels decreased from group I (control) to group II (I/R) (P < 0.05) and increased from group II (I/R) to group III (presulindac + I/R) and IV (postsulindac + I/R) (P < 0.05). The number of apoptotic neurons increased from group I (control) to group II (I/R) (P < 0.05) and decreased from group II (I/R) to group III (presulindac + I/R) and IV (postsulindac + I/R) (P < 0.05). CONCLUSION: The Sulindac may have neuroprotective effects on ischemic neural tissue to prevent the reperfusion injury after ischemia.