[Reaction of ethyl acetoacetate with the hydrazides of some phenoxyacetic acids].
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BACKGROUND AND PURPOSE: Ketone bodies provide important alternate fuel for brain metabolism, and their transport into the brain increases with prolonged fasting. During diabetic ketoacidosis (DKA), serum ketone concentrations markedly increase; however, little is known about whether ketone bodies accumulate in cerebral tissues during DKA. We used proton MR spectroscopy (MRS) to detect cerebral beta-hydroxy butyrate (betaOHB) and acetone/acetocaetate (AcAc) in children with DKA. METHODS: Twenty-five children underwent brain MRS: nine within 4 hours of the start of treatment for DKA; 11, at 4-8 hours; and five, at 8-12 hours. MRS was repeated after their recovery from the DKA episode at > or =72 hours after the start of treatment. MRS was evaluated for peaks corresponding to betaOHB (doublet centered on 1.20 ppm) and lactate (doublet centered on 1.33 ppm). Difference spectroscopy was used to identify the AcAc peak at 2.22-2.26 ppm. RESULTS: betaOHB was detected in 13 children (52%), more frequently within 4 hours (eight children, 89%) than after 4 hours (five children, 31%). AcAc was detected in 15 children (60%), more frequently at >4 hours after the start of treatment (12 patients, 75%) than in the first 4 hours (three patients, 33%). Lactate was detected in five children (18%), all within the first 8 hours of treatment. CONCLUSION: In children, betaOHB and AcAc accumulate in the brain during DKA, and they can be detected on MRS. Care should be taken in interpreting MRS results in patients with DKA to avoid erroneously attributing betaOHB peaks to lactate.
Using 11C-ACAC, 11C-TYR, and 18FDG as tracers, brain uptake of these substrates was studied in cat brain with a freezing lesion, by PET, at 1 day to 3 weeks after injury. Also MRI was conducted. Although the MRI scans depicted the morphological changes, such as edema formation, the PET studies of the brain uptake of substrates visualized the pattern of changes, which in the fresh lesion was largely governed by impairment of the BBB, but in the chronic lesion they were indicative of the proliferation of reactive cells in the process of tissue repair and edema resolution.
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