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Enflurane and isoflurane appeared equally effective in decreasing the efficiency of oxidative phosphorylation in isolated mitochondria, while halothane was twice as effective as these two anesthetics. On the other hand enflurane and isoflurane exhibited different dose-response relationships when the uptake of calcium was measured (with a calcium-selective electrode) or the transmembrane electrical potential was monitored (with tetraphenylphosphonium-selective electrode) during ATP synthesis or calcium uptake in anesthetic treated mitochondria. The results indicate that the effects of isoflurane and enflurane on the mitochondrial energy converting processes are qualitatively, but not quantitatively, analogous to those previously described for halothane. Moreover the damaging action of isoflurane gradually increases as the anesthetic concentration increases, while that of enflurane suddenly increases above a threshold concentration. It appears that the effects of halothane, enflurane and isoflurane on isolated mitochondria involve both the ATP synthetase and the inner membrane permeability barrier, although the membrane-anesthetic interactions responsible for such effects are probably different for each anesthetic.

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The anesthetics halothane, enflurane, isoflurane and 2,6-diisopropylphenol negatively affect several energy-linked processes in isolated rat liver mitochondria, decreasing their efficiency. The adverse effects observed in the presence of halothane, enflurane and 2,6-diisopropylphenol are similar for many aspects although, being caused by anesthetics having different molecular structures, they differ significantly from the quantitative point of view. A relevant role in the anesthetic-induced mitochondrial injuries appears to be played by long-chain acylCoA, whose level is markedly increased in mitochondria incubated in the presence of halogenated anesthetics. In addition, the amount of intramitochondrial calcium may also influence the severity of these injuries.

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The halogenated anesthetics halothane, enflurane and isoflurane inhibit the calcium efflux induced by Ruthenium Red in isolated rat liver mitochondria. The extent of the inhibition is higher for enflurane (approximately 50%) than for either isoflurane (approximately 35%) or halothane (approximately 15%), and does not increase significantly between 0.1 and 0.6-1.0 mM anesthetic. Both the mitochondrial respiratory rate and transmembrane electrical potential are unaffected by the halogenated anesthetics concentrations capable to inhibit the efflux of calcium.

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The effect of anticonvulsant drugs was examined on brain GABA levels and GAD and GABA-T activities. The level of GABA was increased by the treatment with diphenylhydantoin. The drug had no effect on GABA-T activity, whereas GAD activity was inhibited. Carbamazepine increased the GABA level but did not effect GAD and GABA-T activities. Diazepam had no effect on GABA level and GAD activity, whereas it caused a slight inhibition of GABA-T activity. Phenobarbital administration decreased GABA level only at the higher concentration. Clonazepam effected only GAD activity. Some anticonvulsant drugs generally increase brain GABA level; however the lack of correlation with an effect on the GAD and GABA-T activities indicate that other factors than metabolism, such as membrane transport processes, are involved in the mechanism of action of anticonvulsant drugs.

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The effects of some antipileptic drugs on the level of GABA in the mouse brain was studied using standardized chromatographic methods. Diphenylhydantoin and carbamazepine determined a marked increase of the cerebral GABA level, whereas phenobarbital, diazepam a,d clonazepam were without effect. The results seem to indicate that diphenyihydantoin and carbamazepine, by increasing the GABA level, may act through an enchancement of the GABA-ergic transmission.

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The effects of some psychoactive drugs on the level and uptake of GABA in the mouse brain was studied using well standardized procedures, mainely the silica-gel cromatography for determining the GABA content and the brain slices for measuring GABA uptake. It was found that levomepromazine, sulpiride, haloperidol and amytryptiline were without effects on the cerebral level of GABA; it was also found that these drugs do not influence the rates of uptake of GABA by mouse brain slices. Such results do indicate that the psychoactive drugs studied are without effects on the level and uptake of GABA in the brain.

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In a study of the role of taurine in the genesis of epilepsy the effects of metrazol-induced convulsions on the uptake and distribution of taurine in the brain were measured. In vivo we found no significant uptake of taurine in the mouse brain; in rabbit brain in most areas significant taurine uptake was found. The physiological levels of taurine were much higher in mouse brain than in rabbit brain. In vivo the regional levels and the uptake of taurine were not significantly changed after generalized convulsions. Uptake in vivo was lowered in slices obtained from mice treated with metrazol. The lack of effect of metrazol convulsions on cerebral taurine in vivo indicates that further studies are needed to clarify the relationship between taurine, a putative inhibitory transmitter, and epilepsy.

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Like their AKR/J parent, (CBAT6T6 X AKR/J)F1 mice are carriers of endogenous G-MuLV and present a high incidence of spontaneous lymphoma. However, the F1 hybrids do not present the immunological deficits seen in pre-leukemic AKR/J mice since they respond normally to in vitro PHA stimulation and to in vivo LPS immunization. These observations suggest that there is probably no direct relationship between the presence of MuLV and immunological impairment. Studies have been carried out to ascertain whether the altered immunological reactivity seen in AKR/J mice is related to factors intrinsic to the immunocompetent cells or to environmental inadequacy. Thus, (CBAT6T6 X AKR/J)F1 mice were thymectomized, irradiated, reconstituted with syngeneic bone marrow and simultaneous transplant of CBAT6T6 and AKR/J thymus, and their lymphocyte response to PHA was assayed. In addition, antibody production following LPS immunization was studied by transferring AKR/J splenic cells to irradiated CBA6T6 or (CBAT6T6 X AKR/J)F1 mice, and vice-versa. The results of these investigations indicate that an intrinsic lymphocyte hyporeactivity is present in AKR/J mice and environmental factors do not modify the reactivity of the transferred immunocompetent cells.

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The levels of the free amino acids of the mouse brain were studied after convulsions induced by Metrazol; a decrease of level of taurine and a significant increase of level of alanine, phenylalanine and isoleucine were found. The net uptake of L-histidine by the mouse brain in vivo was similar under normal conditions and after Metrazol-induced generalized convulsions; that of L-methionine was much higher after convulsions and there was no uptake of L-aspartic acid, either under physiological conditions or after convulsions. The net uptake of L-histidine by various regions of the rabbit brain in vivo after convulsions was significantly higher than control values in the cortical areas, while that of L-methionine was significantly higher in the subcortical ones; there was no uptake of L-aspartic acid by the rabbit brain in normal condition, whereas after convulsions a small entry seemed to occur in the subcortical areas. These results indicate that cerebral permeability processes of amino acids are somewhat altered during convulsive phenomena, as already described elsewhere for ions andproteins.

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