Abstracts

LOCAL BRAIN HYPOTHERMIA SUPPRESSES PERIFOCAL EPILEPTIFORM DISCHARGES INDUCED BY FOCAL CEREBRAL ISCHEMIA IN RATS

Abstract number : 2.046
Submission category : 1. Translational Research: 1D. Devices, Technologies, Stem Cells
Year : 2012
Submission ID : 16102
Source : www.aesnet.org
Presentation date : 11/30/2012 12:00:00 AM
Published date : Sep 6, 2012, 12:16 PM

Authors :
Y. He, M. Fujii, T. Inoue, S. Nomura, Y. Maruta, Y. Owada, H. Kida, T. J. Yamakawa, T. Tokiwa, T. Yamakawa, M. Suzuki

Rationale: In acute ischemia, high extracellular potassium and excess glutamate release from the ischemic core lead to depolarization and increased metabolic demand in neighboring neural tissues. These conditions induce periodic epileptiform discharges (EDs) and brain injuries. On the other hand, we have reported that focal brain cooling (FBC) terminates EDs in drug-induced seizure models. Therefore, the aim of this study was to investigate whether FBC also has a favorable effect on focal cerebral ischemia in rats. Methods: Healthy male adult Wistar rats weighing 350 ± 50 g were used in the study. All surgical procedures were conducted under the guidelines of the Yamaguchi University School of Medicine. Under general anesthesia, a small craniotomy was made and focal cerebral ischemia was induced with the photothrombosis technique (illumination after intravenous injection of Rose Bengal at 1.3 mg/100 g of body weight in 0.9% sterile saline) in the primary sensorimotor area (SI-MI). An additional larger craniotomy was made in the SI-MI area and FBC was performed at a temperature of 15°C for 5 h. Electrocorticograms (ECoG) were recorded with needle-type electrodes placed on the cortex at the border zone of the ischemic focus for 5 h during cooling and for 1 h after cooling. After recording of the ECoG, rats were sacrificed and the infarct area was measured with triphenyltetrazolium chloride (TTC) staining. Seven rats each were used in the cooling and non-cooling groups. Results: FBC suppressed all the ECoG frequency bands (1-30 Hz) during and after cooling (p<0.05), except for the delta frequency band in the precooling versus rewarming periods. The injured areas (sections at the ischemic core level) in the cooling and non-cooling groups were 0.99 ± 0.30 and 1.71 ± 0.54 mm2, respectively. Lesion size was significantly reduced in the cooling group (p = 0.026). Conclusions: FBC suppresses periodic EDs and has a protective effect on focal cerebral ischemia. These results suggest that FBC has potential for treatment of cerebral infarction.
Translational Research