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Halothane can cause drug induced hepatitis in man, but the mechanism of halothane hepatitis has not been fully understood. It has been proven that halothane is metabolized, in part, by microsomal mixed function oxidase system(MFOS) of the liver and that the induction of MFOS by phenobarbital increases this metabolic pathway. And it has also been suggested that the metabolites of halothane may be toxic. Therefore we performed this experiment using Sprague-Dowley male rats to determine whether microsomal enzyme induction by phenobarbital wouId affect the response of rat liver after halothane administration. The results are summarized as following: 1) Serum glutamic pyruvic transaminase(KGFT) values in helothane-alone group, checked 24,48,72 and 96 hours after halothane administration (0.15ml/100gm body weight with olive oil intraperitoneally) were statistically the same as those of normal control. In contrast, SGPT values in rats with phenobarbital pretreatment (7.5mg/100gm body weight intraperitoneally for 3 days) followed by halothane administration were 59±9, 70±23, 41±15 and 37% 4 Karmen unit/ml, respectively, at 24,48,72 and hours after administration. The former three were significantly increased (p$lt;0.005, p$lt;0.005, and p$lt;0.025 respectively) in comparison with normal control of 318 Karmen unit/ml, and the value of 96 hours was statistically the same as that of control. 2) The histopathological lesions were not significantly different between groups of halothane-alone and phenobarbital pretreatment followed by halothane administration. The pathological findings observed 24 hours after haltothane administration showed microvesicular change in the midzonal and periportal areas of hepatic lobules. Those of 48 and 72 hours consisted of vacuolar changes in the midzonal and periportal areas, occasionally extending to the centrilobular area, and sometimes coalescent. After 96 hours, the vacuolar changes were no longer s en in most areas, leaving only a mild microvesicular change in the midzonal area. 3) The specific activities of cychrome P-450 before and after phenobarbital pretreatment were determined to confirm that the administered dose of phenobarboital was sufficient to induce microsmal enzyme system. They were 0.35±0.03 nmol/mg protein and 0.95±0.3 nmol/mg protein respectively, indicating that microssmal enzyme induction by phenobarbital mav increase the toxic reaction of halothane to the rat liver. In conclusion, it is highly suggested that the toxic reaction plays an important role on the mechanism of halothane hepatotoxicity.
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Purpose: This study was conducted to measure macular ganglion cell-inner plexiform layer (mGC-IPL) thickness in patients with a history of unilateral single attack of acute primary angle closure (APAC) and to compare it with that of unaffected fellow eyes 8 weeks after resolution using spectrum domain optical coherence tomography (SD-OCT). Methods: Medical records of 24 patients with history of first episode of unilateral APAC were reviewed retrospectively. Eight weeks after APAC, mGC-IPL thickness and peripapillary retinal nerve fiber layer thickness were measured with SD-OCT and analyzed in eyes affected by APAC (group 1) and fellow eyes (group 2). Results: There were no significant differences between the groups with regard to best corrected visual acuity, spherical equivalent, central corneal thickness, or axial length (<em>p</em> > 0.05). There were no significant differences in mGC-IPL thickness in the superotemporal, superior, or superonasal sectors (<em>p</em> > 0.05). However, average, inferonasal, inferior, and inferotemporal sectors of group 1 were significantly thinner than those of group 2 (<em>p</em> = 0.002, 0.002, 0.001, 0.001, respectively). In addition, average mGC-IPL difference between affected eyes and fellow eyes showed a statistically significant correlation with attack duration (correlation coefficient = 0.249, <em>p</em> = 0.019). Conclusions: Normalization of elevated intraocular pressure as soon as possible after APAC onset is recommended in order to reduce mGC-IPL loss, and measurements of mGC-IPL thickness can be helpful for follow-up of APAC patients. J Korean Ophthalmol Soc 2014;55(8):1167-1173