고양이의 뇌허혈 - 재관류 모델에서 산화질소 합성효소의 억제가 뇌에너지 대사에 미치는 영향 ; 31P 와 1H 자기공명분광법을 이용한 연구

Background : The effects of the inhibitor of nitric oxide synthase (NOS) in cerebral ischemia have been debated. Recently, it has been suggested that it depends on the amount of the inhibitor used. Therefore, this study was carried out to evaluate the effects of the NOS in the acute ischemia-reperfusion of the cat model using variable amounts of the inhibitor. Methods : Nineteen cats were divided into 3 groups: group 1 (n = 6), 10 mg/kg of N-nitro-L-arginine methyl ester (I.-NAME); group 2 (n = 7), 0.5 mg/kg; group 3 (n = 6), control group. Incomplete global cerebral ischemia was induced by ligation of both carotid arteries with arterial hypotension (―40 mmHg) for 30 minutes followed by 3 hours of reperfusion. The NOS inhibitor (L-NAME), was injected intra- peritoneally 5 minutes before reperfusion. "P and 'H MR spectroscopy were performed. A series of spectra was acquired in the time intervals before ligation, during ischemia, and after reperfusion Results: Phosphocreatine/inorganic phosphate (PCr/Pi) ratios for group 1 were significantly lower than for groups 2 and 3 (P < 0.05), and there was no significant difference between groups 2 and 3. Lactate/N-acetyl aspartate (Lac/NAA) and lactate/creatine (Lac/Cr) ratios at 180 minutes after reperfusion were higher for group l than for groups 2 and 3 (P < 0.05). There were no significant differences in pH and lactate/choline (Lac/Cho) ratios among the 3 groups. Conclusions : It is demonstrated that the effect of the NOS inhibitor is dosage dependent. A high dose (10 mg/kg) of L-NAME seems to have an adverse effect on recovery of the ischemia, but a low dose (0.5 mg/kg) seenm to have no effect. (Korean J Anesthesiol 2000; 38: 340~347)