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Biomedical subjects

G Adám

Publications and source records attributed to G Adám.

At least 37 records · Page 2Linked to original sources
PubMed1986

Blood-brain barrier damage during the acute stage of subarachnoid hemorrhage, as exemplified by a new animal model.

Models have been devised and characterized in the laboratory rat for studying the neuropathology of subarachnoid hemorrhage. Several ways of injecting blood via different routes have been tried; cortical subarachnoid administration is the most reproducible suitable model. The location of injected blood was detected in histological sections. In this rat model for subarachnoid hemorrhage, the arterial blood pressure and the intracranial pressure did not elevate significantly, and the influence of major ischemic components in the development of brain edema could also be ruled out. Measurements performed on the water, electrolyte, and albumin contents of brain tissue have clearly indicated that the brain edema developing in the acute stage of rat experimental subarachnoid hemorrhage could be classified as having a primarily vasogenic component as well. These findings may have implications in the treatment of subarachnoid hemorrhage.

Acute Disease↗
PubMed1985

Kainic acid neurotoxicity: characterization of blood-brain barrier damage.

The alterations in the water, sodium (Na) and potassium (K) contents of the frontoparietal cortex, hippocampus and thalamus as well as the protein permeability of the blood-brain barrier were investigated in rats 4 h after systemic kainic acid administration. Increases in the water and Na contents and a decrease in the K content were observed together with Evans blue extravasation in the thalamus area indicating the development of vasogenic brain edema. Changes observed in the ion contents of the frontoparietal cortex and hippocampus may be due to a general cell membrane permeability damage but are not caused by a primary disturbance of the blood-brain barrier.

Animals↗
PubMed1984

Prevention by macrocortin of global cerebral ischemia in Sprague-Dawley rats.

We have previously shown that dexamethasone protects female Sprague-Dawley CFY rats against global cerebral ischemia induced by bilateral carotid artery ligation. In the present study, macrocortin derived from rat peritoneal cells exposed to dexamethasone was found to exhibit antiphospholipase A2 activity and to provide significant protection against the fatal consequences of carotid artery ligation. These results suggest that the cerebroprotective effect of glucocorticoids may be related to macrocortin production.

Animals↗
PubMed1984

Cerebroprotective effect of dexamethasone by increasing the tolerance to hypoxia and preventing brain oedema in newborn piglets with experimental pneumothorax.

The effect of dexamethasone (DXM) pretreatment in newborn piglets with experimental pneumothorax (EPT) was studied. Neither low DXM doses nor those administered 1 or 2 h prior to the induction of EPT were found to be effective against its course. In contrast, 5 mg/kg of body wt. of DXM given subcutaneously 4 h prior to EPT improved significantly both the tolerance and laboratory data of the animals. The extent of brain oedema, measured 4 h after recovery, was also considerably lowered. Actinomycin D pretreatment prevented almost completely the beneficial effect offered by DXM suggesting the involvement of newly synthesized protein(s) in the cerebroprotective effect of DXM.

Animals↗
PubMed1984

The blood-brain barrier in hypoxia: ultrastructural aspects and adenylate cyclase activity of brain capillaries.

The ultrastructure of brain microvessels, their permeability to serum albumin, the activities of some endothelial enzymes and the effect of histamine were investigated in rats after a prolonged hypobaric-hypoxic treatment. After prolonged hypoxia, the permeation of serum albumin into endothelial cells increased together with the number of pinocytotic vesicles of the endothelium. Intracarotid histamine stimulated this process even further, and its effect was mediated by H2-histamine receptors. After hypoxia the specific activity of capillary alkaline phosphatase and gamma-glutamyl transpeptidase remained unchanged, while that of adenylate cyclase was greatly increased. Histamine did not modify the structure of tight junctions of isolated capillaries of normoxic animals. Both hypoxia- and histamine-induced modification of the brain microvessels were accompanied by an increase of pinocytosis, which may be stimulated by the activation of capillary adenylate cyclase.

Animals↗
PubMed1983

Conditioned modification of viscerosensory evoked potentials during sleep and wakefulness in cats.

The effects of classic conditioning on the viscerosensory evoked potentials (EPs) were studied in twenty cats during wakefulness (W), slow-wave-sleep (SWS) and paradoxical sleep (PS). Four types of the experiment were performed on four groups of animals. Weak, non-painful stimulation of the small intestine or of the left splanchnic nerve was used as conditional stimulus (CS) in all experiments. A painful or non-painful shock on the left radial nerve served as unconditional stimulus (US) which followed the CS with a delay of 500 ms. In the first and second series of experiments, the CS was paired with non-painful or painful CS during W. In the third and fourth types of experiment, weak US was used and conditioning was done during SWS or PS. The evoked responses were recorded from the primary (SI) and secondary (SII) somatosensory and associative (AS) cortex, the thalamus (VPL), hypothalamus (HPT) and dorsal hippocampus (HPC). In each experiment, the stimulus pairings resulted in a complex electrographic conditional response (CR) which included an amplitude increase of the late components of EP's (early CR) and the development of a wave of 500 ms latency (delayed CR). In the second experiment, however, a behavioural CR (limb flexion) also appeared. All these CRs proved to be extinguishable. The recall of CR established during W was successful in SWS. The traces of CS-US pairings during SWS could, however, be elicited only in SWS. Both establishment and recall of CR were unsuccessful during PS. The possible mechanism of the effects originating from an interaction of conditioning and sleep on the viscerosensory inputs of the brain are discussed.

Animals↗
PubMed1975

Synaptosomal fractions of cat cerebral cortex after hypo-osmotic and detergent treatment.

Different synaptosomal fractions were prepared by subcellular fractionation from cat cerebral cortex. The seperated nerve ending fractions differed in both density and osmotic sensitivity. Synaptosomal ghosts were obtained by hypo-osmotic treatment. In the synaptosomal ghost fractions the synaptic areas seemed to be intact morphologically. The morphology of the "synaptic triad" (pre- and postsynaptic membranes and the synaptic cleft) was not affected even by treatment with Triton X-100 non-ionic detergent (0.6%). The solubilizing effect of different concentrations of the detergent was checked in the supernatants and in the insoluble residues. The homogeneity of various subcellular fractions and the effect of the osmotic and detergent treatments are discussed.

Animals↗