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Biomedical subjects

L Lucchi

Publications and source records attributed to L Lucchi.

At least 55 records · Page 3Linked to original sources
PubMed1986

Acid-base balance during biofiltration (BF).

Acid base balance during biofiltration (BF): Six patients on standard acetate hemodialysis (HD) were switched to BF with 1 m2 AN69-S membrane, 12 hours weekly (BF-4h) and, later on, to a stage with 1.2 m2 AN69-S, 9 hours weekly (BF-3h). During BF, in order not to exceed 25 mEq/l in intradialytic arterial HCO3, arterial acid-base was examined hourly and a mean of 178 and 199 mEq of HCO3 respectively were infused in BF-4h and BF-3h. We obtained a better control of acidosis with a reduction of the intradialytic pCO2 decrease and hypoxemia. The amount of HCO3 infused was related to the patients deficit in HCO3 total pool and therefore it can be predicted, to avoid postdialytic alkalosis.

Acetates↗
PubMed1985

Ethanol administration in vivo alters calcium ions control in rat striatum.

The present paper investigates the effect of chronic ethanol treatment administered through drinking water on [3H]nitrendipine binding and 45Ca uptake in rat striatum. The calcium-independent [3H]nitrendipine binding was slightly increased in treated rats, while the calcium stimulation of the binding was reduced to one fifth of the controls. In striatal slices prepared from a similar group of ethanol-treated rats the K+-stimulated 45Ca uptake was greatly reduced. These results are the first evidence of calcium-antagonist binding-site 'plasticity' following an in vivo pharmacological manipulation correlated with a change in calcium ion transport. In addition, the effect of ethanol on calcium-entry regulation may be a mechanism important for the understanding of its neurotoxic action.

Animals↗
PubMed1984

In vivo chronic lead exposure alters [3H]nitrendipine binding in rat striatum.

The effect of lead as a neurotoxic agent has been associated with alterations in calcium metabolism. On this line, the present study shows that lead alters the characteristics of [3H]nitrendipine ([ 3H]NDP) binding to rat striatal membranes. In vitro, lead shares the action of calcium in enhancing [3H]NDP binding although it is more potent on a molar basis. In vivo, lead exposure through drinking water enhances [3H]NDP binding to crude synaptosomal membrane preparations. This effect is lost when membranes are washed with EDTA-EGTA, indicating that the increased binding is due to the persistence of lead in the brain of treated rats.

Animals↗
PubMed1984

Chronic ethanol changes opiate receptor function in rat striatum.

Ethanol produces supersensitivity of striatal delta-opiate receptor sites labeled by [3H]DADLE and [3H]etorphine. The impairment may be ascribed to the diminished enkephalin release detected in rat striatum after chronic ethanol consumption. On the contrary, a lower affinity of striatal mu-opiate receptors results after same ethanol exposure. In fact, the Kd values of [3H]Met-enkephalin and [3H]DHM are enhanced when measured in striata of ethanol-dependent rats. The diverse sensitivity of the various classes of opiate receptors to ethanol may be ascribed to different ethanol effects on enkephalinergic transmission.

Animals↗
PubMed1984

Chronic lead treatment affects dopaminergic control of prolactin secretion in rat pituitary.

The effect of lead exposure on dopaminergic mechanisms regulating prolactin (PRL) secretion was studied in rats by measuring dopamine (DA) and dihydroxyphenylacetic acid hypothalamic concentrations and DA receptor density in the hypothalamus and pituitary of lead-exposed animals. [3H]Sulpiride was used as dopamine receptor ligand. A decrease of dihydroxyphenylacetic acid (DOPAC) hypothalamic concentrations and a decrease of DA receptor density in the pituitary are shown. The decreased [3H]sulpiride binding in the pituitary is consistent with the elevated serum PRL concentrations previously described in lead-exposed rats.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1984

Chronic ethanol treatment changes the number of beta-receptors in rat brain microvessels.

The effect of chronic ethanol consumption on the binding (125I)-iodohydroxybenzylpindolol to beta-adrenergic receptors in rat brain microvessels has been studied. The results show that chronic ethanol treatment increases the number of beta-receptors present in brain microvessels without changing the binding affinity of the binding site for the beta-adrenoceptor ligand. This effect is apparently not associated with changes in peripheral adrenergic tone, since no differences in platelet epinephrine or norepinephrine concentrations were found between ethanol-treated and control animals. An increase in beta-receptor density in brain microvessels might contribute to the alterations of cerebral blood flow and oxygen consumption reported during chronic ethanol intoxication.

Animals↗
PubMed1983

Effect of chronic ethanol treatment on adenylate cyclase activity in rat striatum.

Chronic ethanol consumption induces an increase in striatal adenylate cyclase enzymatic activity but is unable to further potentiate the dopamine stimulated production of cyclic-AMP. In striatal membranes obtained from chronic ethanol-treated rats, apomorphine exerts a more potent inhibition of [3H]spiperone binding when compared with controls, demonstrating that ethanol increases the affinity of the dopaminergic receptors associated with adenylate cyclase activity. In addition, GTP is unable to modify the agonist component of dopamine receptor in membrane exposed 'in vivo' to ethanol. Data are discussed in terms of a derangement of receptor-adenylate cyclase coupling system produced by chronic ethanol treatment.

Adenylyl Cyclases↗
PubMed1983

Ethanol and dopaminergic systems.

Chronic ethanol consumption produces derangements of cell membrane structure, perhaps by changing membrane lipid content. This impairment leads to modification of membrane-related processes. In fact, after chronic ethanol exposure, an increase in striatal adenylate-cyclase activity occurs. On the other hand, dopamine is unable to further potentiate the production of cyclic AMP. This finding demonstrates that the dopaminergic receptor associated with adenylate-cyclase activity is affected by chronic ethanol treatment. In particular, the affinity of the dopaminergic receptor labelled by 3H-Spiperone is enhanced. In addition, the receptor-adenylate cyclase coupling system is impaired after chronic in vivo exposure of animals to ethanol.

Adenylyl Cyclases↗
PubMed1983

Effects of ethanol, given during pregnancy, on the offspring dopaminergic system.

The fetal alcohol syndrome is characterized by a number of abnormalities consisting of a pre- and post-natal growth deficiency, microcephaly, areas of abnormal nerve cell migration in the brain, mental and psychomotor retardation in children of alcoholic women. These findings may be referred as a teratogenic effect of ethanol on the central nervous system. In order to investigate the above ethanol-neurotoxic effect the striatal dopaminergic transmission was studied. The dopaminergic turnover was measured by 3,4-dihyroxyphenilacetic acid content and 3H-Spiperone binding has been carried out to determine dopaminergic receptor alterations induced by chronic ethanol consumption during pregnancy. Our work demonstrates long-lasting modifications of dopaminergic neuronal function after exposure of the experimental animal to ethanol during fetal life. In particular, a decreased receptor function has been observed in rats exposed to ethanol only during the perinatal period. In the same group of rats, diminished receptor activity leads to an enhancement in DOPAC content still detectable after a long period from cessation of ethanol treatment. Neurochemical data are reinforced by behavioral observations. In fact, a significant decrease of spontaneous locomotor activity in the rats chronically treated with ethanol during fetal life was observed. In addition, the altered response of locomotor activity after drug administration may be ascribed to the modified dopaminergic function. With this experimental approach we assume that the action of ethanol on the central nervous system may be a marker of its teratogenic effect.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1982

Neuronal mechanisms regulating ethanol effects on the dopaminergic system.

Chronic ethanol consumption induces an increase in striatal 3H-Spiroperidol and 3H(-)Sulpiride specific binding by enhancing the affinity between the different dopaminergic recognition sites and the labelled ligands. Dopamine (DA) receptor supersensitivity is also suggested by the enhanced effect of neuroleptics in inducing hypomotility in rats treated with ethanol. The results, obtained by means of the administration of neuroleptics in comparison to ethanol treated rats, indicate a lack of cross tolerance between ethanol and other drugs acting on the dopaminergic recognition sites. These data suggest that ethanol effects on the dopaminergic system are mediated by events involving other neurotransmitter systems.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1982

Action of ethanol and salsolinol on opiate receptor function.

Ethanol may act at the enkephalinergic receptor level through condensation products such as salsolinol. This fact has been demonstrated by studying the 'in vitro' and 'in vivo' salsolinol interaction on enkephalinergic receptor sites labeled by [3H-Met] enkephalin. The modification induced by chronic ethanol and salsolinol on this neuronal system is a reduction of the affinity of the receptor for its ligand. These data suggest that a down regulation process due to the continuous opiate receptor stimulation occurs after ethanol administration.

Acetaldehyde↗
PubMed1982

Central toxic effects of chronic ethanol treatment: actions on GABA and benzodiazepine recognition sites.

Prolonged ethanol treatment modifies various neurotransmitter systems. GABAergic neuronal function was particularly affected. On the other hand, clinical reports have indicated an interaction between ethyl alcohol and benzodiazepine receptors. These observations suggest a possible site of action of ethanol at the level of the GABA-benzodiazepine receptor complex. Our results showed that ethanol treatment differentially affected GABA receptor function and benzodiazepine binding sites. When [3H]GABA binding in the cerebellum, striatum and hippocampus was increased, [3H]diazepam binding remained unchanged in the same areas. The possibility of modulation of ethanol effects on GABAergic neurons through benzodiazepine receptors is discussed.

Animals↗
PubMed1981

Chronic lead treatment induces in rat a specific and differential effect on dopamine receptors in different brain areas.

There is now evidence that two classes of dopaminergic receptors are present in CNS of the rat: D1, associated, and D2, not associated with adenylate cyclase activity. Drugs which interact specifically with D2 receptor are more capable of antagonizing the hyperkinetic behavior induced by lead exposure in rat. They also have a beneficial effect in children with hyperkinetic disorders. We found that the dose (-)sulpiride which causes sedation is lower in lead intoxicated animals than in controls. On the contrary, haloperidol produces sedation with the same potency in lead-treated and in control rats. The reported behavioral effects were found to be correlated with biochemical changes. In fact, in lead exposed rats D2 receptors, measured by (-)-[3H]sulpiride stereospecific binding, are altered, while D1 receptors seem not to be affected. The alterations are different according to the area examined: D2 receptor function is increased in the striatum and decreased in the nucleus accumbens. The impairment of D2 receptor might explain the better capacity of substituted benzamides to improve the hyperkinetic behavior observed in lead exposed rats.

Adenylyl Cyclases↗
PubMed1980

Aging process affects a single class of dopamine receptors.

[3H]Spiroperidol and [3H](-)-sulpiride specific binding have been used to assay for D1 and D2 dopaminergic recognition sites in striatal membranes of aged rats. While [3H]spiroperidol binding shows a decreased number of binding sites, no changes have been detected in [3H](-)-sulpiride binding, which is a marker for D2 dopaminergic receptors. Data obtained with GTP and DA-dependent adenylyl cyclase activity confirm the hypothesis that aging selectively affects in rats those dopaminergic receptors coupled to the formation of cyclic AMP (D1).

3,4-Dihydroxyphenylacetic Acid↗