In vivo proton nuclear magnetic resonance spectroscopy was utilized to determine whether lactate is preferentially utilized as metabolic fuel by the neonatal dog brain. The data showed that during lactate influx, metabolism of lactate could account for most of the fuel needed for oxidative metabolism. The in vivo nuclear magnetic resonance measurements were corroborated by conventional arteriovenous determinations which showed steep decline of arteriovenous difference of glucose and shaφ increase in arteriovenous difference of lactate during lactate infusion.

ABSTRACT. The purpose of these experiments was toEarlier investigations in the adult rat disclosed that there is a determine whether flurothyl-induced status epilepticus rapid fall in PCr and pH, as well as a rise in lactate within 5 min causes progressive decline of brain high-energy phosphates of onset of status epilepticus. Thereafter, a new steady state for and progressive increase in brain lactate in neonatal dogs PCr and lactate was established (4-8). However, these studies in who are paralyzed and oxygenated. In vivo 31P nuclear adult experimental animals could not accurately follow the semagnetic resonance spectroscopic measurements showed quential changes in the same animal for a prolonged period of that the fall in brain pH occurred early in the course of time, but rather relied upon measurements made in multiple seizure. The decline in phosphocreatine was more gradual, groups of animals. Moreover, differences in blood-brain permei.e. 50% reduction, during the 1st h of seizure. There was ability to lactate (9-13) make it difficult to extrapolate data no reduction in ATP during the 3 h of status epilepticus. obtained in the adult to the neonate. In vivo 'H nuclear magnetic resonance measurement ofIn the present study, seizure was induced with the convulsant brain lactate disclosed a steep rise that stabilized by 60 gas flurothyl (bistrifluoroethyl ether) to avoid parenteral adminmin. Brain and blood lactate were closely related during istration of acidic convulsants such as bicuculline or kainic acid. the initial phase of seizure, suggesting rapid efflux of The metabolic effects of flurothyl are of interest because flurothyl lactate from brain or systemic production of lactate. Blood retards brain growth in the neonatal rat (14), and produces lactate exceeded brain lactate after 1 h of status epilepticus. neuronal necrosis in the adult rat (1 5). Three types of studies The new steady state for cerebral phosphocreatine and were performed: in vivo 31P NMR to determine brain high-energy lactate during status epilepticus was achieved much more phosphate metabolism and brain pH; in vivo 'H NMR to measslowly during neonatal status epilepticus than has been ure brain lactate; and in vitro 'H NMR spectroscopy to quantitate reported during status epilepticus in the adult experimental concentrations of PCr, ATP, lactate, glucose, and amino acids. GABA, y-aminobutyric acidThereafter, ventilator settings were not changed. Muscle paralysis was maintained throughout the experiment by parenteral administration of pancuronium bromide. To reduce pain, animals were ventilated with 30% 02/70% N 2 0 and topical anesthetic (lido-NMR spectroscopic studies in human neonates (1) as well as caine jelly, 1%) was applied to all incision sites. During status in neonatal experimental animals (2) show that brief seizures epilepticus, loss of awareness was produced by the seizure itself. reduce levels of PCr and elevate levels of inorganic phosphate in EEG and blood pressure were monitored continuously with a brain, but do not pertu...

No abstract

No abstract

Using in vitro microdialysis, we tested the hypothesis that anoxia-induced release of excitatory amino acids is greater in adult rat brain than in turtle brain. Ten minutes of anoxia produced significant elevation of glutamate (from 0.39 +/- 0.03 to 0.90 +/- 0.18 microM dialysate, means +/- SE, P < 0.05), aspartate (from 0.28 +/- 0.12 to 1.20 +/- 0.49 microM, P < 0.05), glycine, and alanine in the rat brain slice. During reoxygenation, alanine and glycine returned toward baseline values, whereas aspartate and glutamate remained elevated. In contrast, prolonged anoxia (60 min) in the turtle brain slice resulted in only minimal increase in aspartate (from 0.06 +/- 0.01 to 0.09 +/- 0.02 microM, P < 0.05) and, interestingly, a decrease in glutamate (from 0.50 +/- 0.11 to 0.33 +/- 0.09 microM, P < 0.05). Levels of glycine, alanine, and taurine were unchanged. We conclude that oxygen deprivation causes marked increase in excitatory amino acids in the anoxia-sensitive rat brain slice, while oxygen deprivation for an even longer period of time in the turtle brain slice produces substantially less change. We speculate that the difference in sensitivity to anoxia between rat and turtle is at least partly attributable to the major difference in interstitial levels of excitotoxic amino acids during oxygen deprivation.