Carbonyl reduction of 6-tert-butyl-2,3-epoxy-1,4-benzoquinone, a metabolite of 3-tert-butyl-4-hydroxyanisole, by rat liver microsomes and cytosol.
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Biomedical subjects
Publications and source records attributed to K Tajima.
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OBJECTIVE: The objective of this study was to compare the plasma alcohol concentrations after celiac plexus block in different types of cancer. The authors studied the consecutive changes of plasma alcohol concentrations after celiac plexus block in a gastric cancer group (group 1, n = 6) and a pancreatic cancer group (group 2, n = 5). METHOD: Celiac plexus block was performed with 10 ml of absolute ethyl alcohol. In all patients, operations had been performed 1.2-3.5 years before the block. Arterial blood was sampled at 0, 5, 10, 15, 30, 60, 120, 240, and 480 minutes after the block. RESULTS: The average dose of absolute ethyl alcohol was 0.186 g/kg in group 1 and 0.182 g/kg in group 2. Plasma alcohol concentrations in group 1 were about four times greater than those of group 2 (p < 0.01). The mean maximum level was reached at 15 minutes after injection in group 1 (44.0 +/- 5.8 mg/dl) and at 30 minutes in group 2 (13.1 +/- 2.4 mg/dl). CONCLUSION: Plasma alcohol concentrations after celiac plexus block showed different patterns according to the site of cancer and the type of operation performed.
The effect of MET-88 [3-(2, 2, 2-trimethylhydrazinium) propionate], a gamma-butyrobetaine hydroxylase inhibitor, on the ischemic changes of energy metabolism was studied in the anesthetized dog. In the dog pretreated orally with MET-88 (50, 100 or 200 mg/kg/day) or placebo for 10 days, the left anterior descending coronary artery was occluded for 60 min, and the myocardium was taken from the left anterior descending coronary area (ischemic area) and left circumflex area (nonischemic area) for metabolic analysis. In the ischemic area, occlusion of the left anterior descending coronary artery decreased the tissue levels of adenosine triphosphate, adenosine diphosphate and creatine phosphate, increased the tissue levels of adenosine monophosphate and lactate, and decreased the value of the energy charge potential. These metabolic alterations, induced by occlusion of the left anterior descending coronary artery, were dose-dependently attenuated by MET-88. In the nonischemic area, MET-88 did not markedly change either the tissue levels of energy metabolites or the value of the energy charge potential. These results indicate that MET-88 attenuates the derangement of the energy metabolism in the ischemic myocardium, without affecting the energy metabolism in the nonischemic myocardium.