Biomedical subjects

M Baraldi

Publications and source records attributed to M Baraldi.

95 records · Page 6Linked to original sources

PubMedDate not supplied

Endogenous benzodiazepines.

The existence of endogenous benzodiazepines such as diazepam and nordiazepam has been provided in human blood and brains as well as in medicinal plants and foods. It must be stressed, however, that in plasma and brain tissue there are also other benzodiazepine-like compounds termed 'endozepines' which are not halogenated. A synthetic pathway for the production of benzodiazepine-like compounds and endozepines has not yet been found, hence it may be surmised that these compounds could be of exogenous source. Changes in the level of endogenous circulating benzodiazepines due to food or drug ingestion could be responsible for pathological conditions. Clinical experiments were designed in order to study the levels of the endogenous benzodiazepines in vegetables and in the blood of control subjects and of cirrhotic patients. These patients accumulate benzodiazepines because of decreased liver metabolization capacity and impaired renal secretion, reaching plasma concentrations similar to those recorded in commercial benzodiazepine consumers.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMedDate not supplied

Urine retention due to intra-spinal cord injection of colchicine in rats: improved recovery of bladder function by monosialoganglioside GM1 and nerve growth factor administration.

Intra-spinal cord injection of a low dose of colchicine (2 micrograms/rat) at the lumbar level affects the micturition reflex leading to voiding suppression, bladder hypertrophy and overflow incontinence which lasts about four weeks. The administration of nerve growth factor and monosialoganglioside GM1 normalizes urine output within 3 days and improves recovery of the bladder contraction tested by a cystometric analysis.

Animals↗

PubMedDate not supplied

Follow-up of methylmercury concentration in brain areas of developing rats exposed during prenatal life using cold-vapor absorption spectrometry.

The concentration and the distribution of mercury in six different brain areas of developing rats (21 and 60 days of age) exposed to methylmercury (MMC) during prenatal life were determined by using pressure decomposition of the tissues and cold-vapor atomic absorption spectrometry. The distribution of mercury in brain samples showed that the metal distributes to all brain areas, but with different levels. The amount of mercury in the brain areas was about 10-100 times higher, depending on the tested area, in MMC exposed rats than in control, at day 21 of age, while it was practically equal to controls at 60 days of age. These data seem to be of importance in order to correlate the presence of mercury in the brain and its distribution to brain areas after a single exposure to MMC with transient or permanent changes in specific neurotransmitter system and altered behaviors.

Animals↗

PubMedDate not supplied

Neurobehavioral and neurochemical abnormalities of pre- and postnatally lead-exposed rats: zinc, copper and calcium status.

Although diverging opinions have been expressed, there is a body of evidence of a cause-effect relationship between chronic exposure to lead and altered behavior in children. There are several problems in the interpretation of the behavioral and biochemical anomalies described in experimental models of lead intoxication due mainly to the different experimental conditions used. One of the major criticisms is linked with the claim that in several studies too high levels of exposure were used, hence inducing the suspicion that the effects specifically attributed to lead intoxication could be related to unspecific actions. Here we report that, using an experimental model of pre- and postnatal intoxication of rats exposed to a very low amount of lead (1 mg/kg/day), in parallel with behavioral anomalies, there are slight changes in cerebral dopaminergic and GABAergic receptors. A new finding was the discovery that in this condition there is a markedly increased number of opiate receptors in the hypothalamus (and other brain areas) in parallel with a decrease of beta-endorphin and an increase of Met-enkephalin. Therefore, low levels of lead intoxication which could be pertinent to the human situation, seem to induce neurotoxic effects which may be responsible for the behavioral anomalies in rats and, maybe, in children.

Animals↗

PubMedDate not supplied

Distribution of [3H]colchicine in brain and spinal cord areas following its intracerebroventricular or intra-spinal cord injection in rats.

Intracerebroventricular or intra-spinal cord (at lumbar level) injection of low doses of colchicine leads to irreversible urine retention. To learn whether colchicine induces this effect by diffusing from the sites of injection, we studied, using the above-mentioned routes of administration, the distribution of [3H]colchicine in brain and spinal cord areas as a function of time. The release of [3H]colchicine into the blood and its elimination via the renal route was studied as well. The results of these experiments show that after its intracerebroventricular injection, [3H]colchicine diffuses to brain areas that normally exert a facilitatory or inhibitory action on urine excretion but reaches the lumbar region in only modest amounts (0.02%). On the other hand, after its intra-spinal cord injection, [3H]colchicine remains at the site of injection, where the sacral micturition center is located. This suggests that intracerebroventricular or intra-spinal cord injected colchicine induces urine retention by exerting its action at two different levels of the neuronal pathway that regulates micturition, depending on the site of injection.

Animals↗