Objectives: Surgeries can trigger stress responses including metabolic and hormonal changes. It is important to suppress stress response during surgery. We compared the effects of isoflurane and sevoflurane on surgical stress in intracranial tumor surgery. Methods: Thirty ASA physical status I, II, III patients, scheduled for elective craniotomies, were enrolled in this prospective, randomized study. Anesthesia was induced with sodium thiopental fentanyl and vecuronium bromide and maintained with a 50% oxygen-air mixture along with isoflurane or sevoflurane. Venous blood was sampled to measure cortisol, ACTH and prolactin levels 24 hours before surgery, 1 min before anesthesia induction, during tumor removal, 1 min after extubation, at 3, 6, 12, 24, 48 hours. Results: There was no statistically significant difference between two groups regarding demographic characteristics of patients. In group I, ACTH levels were significantly higher 1 min after extubation, at 3 and 6 hours. In Group S, significant increases were observed during tumor removal, 1 min after extubation, at 3 and 6 hours. Cortisol levels were significantly higher in both group after tumor removal, 1 min after extubation, at 3, 6, 12 and 24 hours. Prolactin levels were significantly higher in Group I during tumor removal, after extubation, at 3 and 6 hours. In group S, significant increase in prolactin level was observed only during tumor removal and 1 min after extubation. There were no significant differences in ACTH, cortisol and prolactin values between the two groups. Conclusions: Using isoflurane or sevoflurane for anesthesia during intracranial tumor surgery are not superior to each other regarding hemodynamic and hormonal stress response.
P atients undergoing intracranial surgery are at risk for cerebral ischemia. Therefore, the aim of neuro-anaesthetics is to provide adequate cerebral perfusion during surgery [1]. In patients with increased intracranial pressure (ICP), due to cerebral tumors it is accepted that volatile anaesthetic agents are effective in the protection of cerebral ischemia that may develop due to decrease in systolic arterial pressure (SAP) [2]. Isoflurane's cerebral protection mechanisms include reduction of cerebral metabolic rate (CMR) and metabolic suppression, inhibition of sympathetic activity, reduction of glutamate receptors which are prevent calcium flow, and suppression of excitotoxicity of calcium cascade [3]. It is thought that isoflurane may be secondary to direct vasodilatation or to reduction in CMR by the increase in cerebral blood flow (CBF) reduction [4]. Isoflurane has been reported to cause cerebral protection similar to barbiturates by depressing CMR, and it was shown that it reduce ceree
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