Biomedical subjects

Antonio Paparelli

Publications and source records attributed to Antonio Paparelli.

22 records · Page 2Linked to original sources

PubMed2002

Morphological alterations induced by loud noise in the myocardium: the role of benzodiazepine receptors.

Noise represents an environmental stress factor affecting several organs and apparati, including the cardiovascular system. In experimental animals undergoing noise exposure, subcellular myocardial changes have been reported, especially at mitochondrial level; in particular, after 6 hours of exposure only the atrium exhibited significant mitochondrial alterations, whereas after 12 hours as well as subchronic exposure both atrium and ventricle were damaged. The first part of the present article overviews the experimental evidence on effects of noise on the myocardium. In the second part, the review analyzes the role of benzodiazepine receptors and the potential efficacy of benzodiazepine ligands in preventing the mitochondrial damage induced by noise exposure. Drugs acting at both central and peripheral benzodiazepine receptors significantly prevent this damage. Differences in the amount and the duration of the protective effect might depend on variability in the potency and pharmacokinetics of the specific drug. The effects of the combined treatment with selective and non-selective peripheral benzodiazepine ligands on noise stimulation are discussed at biochemical level reviewing studies on the effects of noise exposure on mitochondrial fractions.

Animals↗

PubMed2002

Morphological effects in the mouse myocardium after methylenedioxymethamphetamine administration combined with loud noise exposure.

Early toxicity occurring during or immediately after 3,4-methylenedioxymethamphetamine (MDMA, or "ecstasy") administration has not been investigated in detail, although in humans it is responsible for marked side effects, and even death. Acute toxicity induced by MDMA produces rhabdomyolysis involving the myocardium (myocytolysis). Cardiac symptoms, such as tachycardia, hypertension, and arrhythmia, are present to a variable extent in humans abusing ecstasy. In most cases, this substance is abused in the presence of loud noise, which may affect the myocardium. Despite the frequency of the concomitant exposure to ecstasy and loud noise, and the similarities between the early side effects of these two agents, to our knowledge no study has investigated the role of loud noise in modulating MDMA toxicity. Therefore, in the present study, we evaluated whether cardiac effects of MDMA administration following a typical "binging" pattern are enhanced by concomitant exposure to loud noise. We selected low doses of MDMA in order to avoid gross morphological alterations, or lesions detectable under light microscopy. The myocardial alterations observed were visible only at the ultrastructural level. We found a dramatic enhancement of alterations in the mouse heart upon MDMA administration during loud noise exposure. Remarkably, this enhancement was evident both as a decrease in the threshold dose of MDMA necessary to alter the myocardial ultrastructure, and as an increase in myocardial alterations produced by a higher dose of MDMA.

Animals↗

PubMed2002

Ecstasy during loud noise exposure induces dramatic ultrastructural changes in the heart.

The acute toxicity induced by 3,4-methylenedioxymethamphetamine appears as rabdomyolysis involving the myocardium (myocytolysis) and it is often suspected to be responsible for sudden death. In line with this, cardiac symptoms such as tachycardia, hypertension, and arrhythmia are present in persons abusing ecstasy. In most cases, ecstasy is abused in loud noise, which in itself might affect the myocardium. To our knowledge no study has investigated the concomitant exposure to ecstasy and loud noise in order to evaluate the role of the loud noise in modulating MDMA toxicity. In the present study, we analyzed whether cardiac effects following a typical "binging" pattern of MDMA administration are enhanced by concomitant exposure to loud noise. Our findings did not show any myocardial lesion detectable under light microscopy. In contrast, alterations were visible at the ultrastructural level as mitochondrial changes. In particular, we found a marked enhancement in the number of altered mitochondria when MDMA was administered during exposure to loud noise.

Acoustic Stimulation↗

PubMed2002

Brief and repeated noise exposure produces different morphological and biochemical effects in noradrenaline and adrenaline cells of adrenal medulla.

Exposure to stressful stimuli is known to activate the peripheral sympathetic nervous system and the adrenal gland. In this study, we evaluated the effects of single or repeated bouts of exposure to a readily measurable stressful stimulus (loud noise) on the catecholamine content and ultrastructure of the rat adrenal medulla. In particular, we measured tissue levels of dopamine, noradrenaline, adrenaline and metabolites. In parallel studies, we evaluated the fine ultrastructure of catecholamine cells, including a detailed study of catecholamine granules and a morphometric analysis of adrenaline and noradrenaline medullary cells. Animals were exposed either to a single (6 h) session of loud (100 dBA) noise, or to this noise stimulus repeated every day for 21 consecutive days. There was a marked correlation between biochemical indexes of catecholamine activity and the ultrastructural morphometry of specific catecholamine granules. Exposure to loud noise for 6 h induced a parallel increase in dopamine, noradrenaline, adrenaline and their metabolites, a polarization and an increased numerical density of noradrenaline and adrenaline granules in the cells. After repeated noise exposure, noradrenaline levels were significantly higher than in controls, and adrenaline decreased significantly. In addition, adrenaline cells also exhibited ultrastructural alterations consisting of wide homogeneous cytoplasmic areas and large, pale vesicles.

Adrenal Medulla↗