The effect of ketamine on cortical spreading depolarization inmice subarachnoid hemorrhage model which is done by filament perforationmethod

The subarachnoid hemorrhages due to life-threatening bleeding of intracranial aneurysms are responsible for %5 of all strokes. They cause a high socio-economical burden due to occurrence at a younger age and high mortality rate. %15 of patients who has an aneurysmal subarachnoid hemorrhage die before hospital arrival. %25 of in-hospital mortality occurs in the first 24 hours. Despite successfully closed aneurysms, the remaining %60 patients are at high risk because of brain damage caused by first bleeding and ongoing pathophysiological processes. The main cause of mortality in these patients that have shown many years ago is diffuse cerebral infarcts and it is thought that the reason is large arterial spasm which occurs 3-15 days after bleeding. In recent years, the thought about the only reason for mortality and morbidity after subarachnoid bleeding is vasospasm is been in doubt. In 2004, for the first time, the concept of early brain injury was found to explain acute pathophysiological events which occur in the first 72 hours in patients who had a subarachnoid hemorrhage, before the occurrence of vasospasm. After the start of subarachnoid hemorrhage, in a short time (approximately 15 minutes), despite it being related to the size of the hematoma, the intracranial pressure returns to before hemorrhage or at proximate values. There are several types of research about microcirculation problems that cause cerebral ischemia, defect of the blood-brain barrier, cortical spreading depolarization, and excitatory neurotransmitters such as glutamate might be responsible for early brain injury. Cortical spreading depolarizations are cortical depolarization waves that spread at speed of 2-6 mm per minute. In normal neurons, after cortical spreading depolarization, repolarization accompanies by an increase in local blood flow. In bleeding brains, cortical spreading ischemia accompanies depolarization. The effect of cortical spreading depolarization on early brain injury and its relationship with bad prognosis is supported by animal and human research. Researches about drug effects v in cortical spreading depolarization models have great importance in the development of new medical treatments. In addition to the hard passage of therapeutic substances from the blood-brain barrier, rapid metabolization of drugs and clearance from the blood which affect the central nervous system, are important obstacles to the invention of central nervous system drugs. In this research, the effect of ketamine anesthesia on cerebral blood flow is studied in a mice model with a filament perforation method. In this experiment, 3 groups of Swiss albino mice have used. A subarachnoid hemorrhage model in mice has been created with the filament perforation method. In every three groups of mice, under the laser speckle imaging, the number of cortical spreading depolarization waves have been examined before the procedure, after the procedure and 24 hours after the procedure and mice have sacrificed. The subarachnoid hemorrhage models in mice have formed with the filament perforation method, under isoflurane anesthesia in the isoflurane group and ketamine anesthesia in the ketamine group. In the sham group, the filament has taken forward through the external carotid artery however perforation has not been created in two mice under isoflurane and in two mice under ketamine anesthesia. There have been 8 mice in the isoflurane group, 8 mice in the ketamine group, and 4 mice in the sham group. In a subarachnoid model in mice with filament perforation method under ketamine anesthesia have better cerebral blood flow compared with subarachnoid hemorrhage model with filament perforation method under isoflurane anesthesia. Key Words: subarachnoid hemorrhage, cerebral blood flow, laser speckle imaging, ketamine, isoflurane.