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  • Title: MRI and MRS studies on acute effects of ethanol in the rat brain.
    Author: Hirakawa K, Uekusa K, Sato S, Nihira M.
    Journal: Nihon Hoigaku Zasshi; 1994 Apr; 48(2):63-74. PubMed ID: 8196210.
    Abstract:
    Magnetic resonance imaging and spectroscopy (MRI and MRS) were used to examine the effects of intoxicating doses of ethanol on the rat brain. 1H-MR images were obtained using three different methods: (1) PD weighted images, (2) T1 weighted images and (3) T2 weighted images. T1 and T2 relaxation times of the tissues were calculated by pixel-to-pixel image computation. After ethanol treatment, the cerebral hemispheres showed high signal intensities in the T1 weighted images, whereas low signal intensities were observed in the T2 weighted images, markedly in the cortex. At 4 h, the T1 values significantly decreased in the thalamus and the hypothalamus of the ethanol treated rats compared with those of the animals under pentobarbital anesthesia. At 1 h, the T2 values significantly decreased in the cortex of the ethanol treated rats. At 4 and 24 h, the T2 values significantly decreased throughout the cerebral hemispheres in the ethanol treated rats. The in vivo 31P-MRS results showed that after ethanol treatment, ATP and phosphocreatine slightly decreased, but not to a great degree. Intracellular pH levels, determined using the values of the chemical shift in inorganic phosphate peaks, decreased and returned to normal by 4 h. In the highly sedated animals, the acidosis observed early on was followed by heavy alkalosis. In in vitro 1H-MR spectra of brain and blood extract samples, many kinds of metabolites were assigned. The quantitative results were as follows: (1) Blood and brain ethanol levels rose to a peak at 1 h after ethanol treatment and no ethanol was detected at 24 h in any samples. (2) Blood acetate levels increased significantly, and returned to the control level by 24 h, whereas the brain acetate levels were largely unchanged. (3) Blood lactate levels decreased significantly at 0.5 h and brain lactate levels mildly increased and rose to a peak at 2 h. (4) Brain N-acetylaspartic acid (NAA) increased at 0.5 h significantly and decreased significantly at 4 h. Electron microscopic findings were as follows: (1) Both neuronal and glial cells were edematous after ethanol treatment. (2) Congestion was serious in all the regions we observed, and it was still present 24 h after ethanol treatment. (3) Swelling of mitochondria was observed in capillary endothelial cells. Our results suggest that high doses of ethanol cause circulatory disorders in the rat brain and disturb the water balance in the cerebral tissues, changing the structures of intracellular water molecules. It also causes metabolic confusion without depletion of high energy phosphate metabolites.
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