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Biomedical subjects

A Bertelli

Publications and source records attributed to A Bertelli.

At least 73 records · Page 4Linked to original sources
PubMed1992

Intraspinal degenerative atrophy caused by sciatic nerve lesions prevented by acetyl-L-carnitine.

Peripheral nerve lesions cause retrograde changes in the spinal cord, involving initially the descending serotoninergic pathways and later the substance P sensory input and methionine-enkephalin interneurons. Within 48 h after sciatic nerve resection there is a significant increase of 5-hydroxyindoleacetic acid in the lumbar spinal cord with no changes of serotonin metabolism in the cell body areas. The immunocytochemical analysis of the spinal cord shows that 20 days after nerve lesion there is a loss of substance P-positive boutons in the laminae I and II of the dorsal horn in the lumbar segment. Such a morphological change is correlated by radioimmunoassay for substance P and methionine-enkephalin, that reveals a significant loss of both peptides. Treatment with acetyl-L-carnitine prevents the early 5-hydroxyindoleacetic acid increase and the reduction of peptide content observed 20 days after lesioning the sciatic nerve. These data suggest that treatment with acetyl-L-carnitine exerts a neuroprotective activity preventing the retrograde changes triggered by peripheral nerve lesions.

Acetylcarnitine↗
PubMed1992

Prevention and control of surgical infections.

Surveillance and control of hospital infections are two particularly important aspects of the surgical ward, and great activity is necessary in the identification and the elimination of the risk factors whenever possible. Today the rational use of antibiotics, in both the prevention and treatment of infections, should be used to avoid or limit nosocomial infections, and it is as important as the use of disinfectants. Cefotetan has been studied in different surgical specialties in prophylaxis and treatment of postoperative infections for its particularly broad spectrum of activity, covering both aerobic and anaerobic organisms, and for the very low incidence of side-effects. In general surgery, Cefotetan has proved able to reduce not only the occurrence of surgical wound infections, but also that of postoperative infections of the genitourinary system.

Cefotetan↗
PubMed1992

Role of endothelin-1 in carrageenin-induced inflammation.

Many vasal factors are produced during an experimental model of inflammation such as rat-paw oedema induced by carrageenin. We investigated whether among the other well-known mediators of inflammation, i.e. serotonin, PAF, eicosanoids and kinins, the peptide endothelin-1 is produced by this kind of inflammatory process caused by carrageenin. Our results indicated that plasma endothelin, and the tissue concentration of endothelin in the oedematous paw, is increased as compared to the control. Consequently, endothelin should also be considered as an important factor in inflammatory processes.

Animals↗
PubMed1992

L-carnitine and coenzyme Q10 protective action against ischaemia and reperfusion of working rat heart.

The protective effect of L-carnitine, coenzyme Q10 and their combination on haemodynamic and metabolic variables has been investigated in isolated perfused working rat hearts after 10 min of global normothermic ischaemia followed by 60 min of reperfusion. In untreated rats or in rats treated only with L-carnitine or with coenzyme Q10, this experimental condition did not induce any irreversible myocardial injury as measured by leakage of cardiac enzymes; however, it decreased some haemodynamic parameters such as cardiac output and minute work, as well as the ATP concentration and the total adenine nucleotide pool. No variations in haemodynamic and metabolic parameters were observed in the rats treated with L-carnitine plus coenzyme Q10. In the perfusate of the hearts of the rats treated with both compounds, a lower purine release (a good index of myocardial energy balance) was also obtained. Although the molecular mechanisms remain to be defined, it appears that the association of L-carnitine and coenzyme Q10 is more effective than using these compounds separately. The complementary and synergic actions of L-carnitine and coenzyme Q10 on metabolism and against peroxidation by oxygen reaction species may explain the efficacy of their association.

Animals↗
PubMed1992

Effect of carnitine and coenzyme Q10 on the calcium uptake in heart sarcoplasmic reticulum of rats treated with anthracyclines.

The effect of the association of carnitine and coenzyme Q10 on doxorubicin cardiotoxicity has been investigated. The two drugs administered to rats for two weeks have lower protective activity when they are administered separately rather than given in association (carnitine 200 mg/kg/day, coenzyme Q10 10 mg/kg/day) for the acute toxic effect of doxorubicin on perfused functioning isolated hearts. The sarcoplasmic reticulum damage measured by calcium-uptake is lower in rat hearts treated with the combined drugs. Deferoxamine and phosphocreatine, two compounds which protect from peroxidative damage due to iron and copper ions, show very strong protection from acute doxorubicin toxicity in isolated perfused hearts. Carnitine and coenzyme Q10 do not protect sarcoplasmic reticulum from iron ions damage, suggesting that their mechanism of protection is not directly related to peroxidation due to metal ion-dependent cardiotoxicity of doxorubicin.

Animals↗
PubMed1992

Effect of ethanol chronic use on hepatotoxicity in rats exposed to tetrachloroethylene.

Tetrachloroethylene, an industrial halogenated solvent, shows several toxic effects. Also at hepatic level this substance can induce a damage but this effect is present only after high exposure, but such high levels have not been found in work environments. Using Wistar rats, we wanted to check whether the chronic administration of ethyl alcohol can modify the action of tetrachloroethylene. Tetrachloroethylene was administered by aerosol and alcohol at the concentration of 15% in drinking water. We observed an increase in plasma triglycerides, and evident histological alteration as a result of steatosis, in rats drinking alcohol as compared to a control group; the administration of tetrachloroethylene to rat drinkers of alcohol did not cause an increase in plasma triglycerides and steatosis as compared to rat drinkers of alcohol, but on the contrary we observed a decrease in alcohol-induced liver damage.

Animals↗
PubMed1992

Perinatal exposure to ethanol affects postnatal degeneration and regeneration of serotoninergic pathways in the spinal cord.

It has been reported that chronic ethanol exposure during intrauterine life may cause severe adverse effects in early infancy that have been termed fetal alcohol syndrome. These alterations may perturb the normal brain development as though alcohol exposure might have altered the basic cellular interrelationship underlying neuronal plasticity. The neonatal lesion of the serotoninergic pathways in the central nervous system with the selective neurotoxin 5,7-DHT supplies an ideal model for studying the effects of substances of abuse on degenerative and regenerative events. The authors' data indicate that perinatal exposure to ethanol (3% in drinking water) causes a more rapid degeneration of the serotoninergic pathways affected by 5,7-DHT; conversely, regeneration and reinnervation of the lumbar spinal cord are markedly improved by ethanol exposure. These results suggest that perinatal ethanol exposure promotes cellular changes that at later stages are capable of improving neural repair in the brain.

5,7-Dihydroxytryptamine↗
PubMed1992

Protection of isolated perfused working rat heart from oxidative stress by exogenous L-propionyl carnitine.

The effect of exogenous L-propionyl carnitine on peroxidative injury was investigated on isolated working rat hearts. The addition of 190 microM hydrogen peroxide to the perfusion buffer caused a marked decrease in aortic flow, minute work and peak aortic pressure, and a release of intracellular enzymes. In the presence of L-propionyl carnitine the haemodynamic damage was significantly lower and enzyme leakage remarkably decreased. The protection was concentration-dependent and the whole structure of the molecule was required, since carnitine alone was found less effective and propionate had no effect. In the absence of hydrogen peroxide L-propionyl carnitine increased heart performance. The effect of L-propionyl carnitine on oxidative stress could account for the beneficial effect of this substance in different models of ischaemic injury. L-propionyl carnitine increases the cardiac performance and protects the rat heart from peroxidation through metabolic and antiperoxidative mechanisms.

Animals↗
PubMed1992

Adenosine and carnitine derivatives and calcium movements in rat heart sarcoplasmic reticulum.

Many researches indicate that some Ca antagonists modulate Ca fluxes not only at the level of the cytoplasmic membrane but also across the sarcoplasmic reticulum. The present study investigates whether certain compounds like propionylcarnitine or acetylcarnitine which have the capacity to influence cardiac activity might interfere with intracellular Ca movements. The results demonstrate that acetylcarnitine and propionylcarnitine do not affect the calcium intracellular movement in sarcoplasmic reticulum.

Acetylcarnitine↗
PubMed1991

Tolerability and safety of clodronate therapy in bone diseases.

A review is made of 126 publications on clinical studies concerning the use of clodronate in the therapy of bone disease involving 1930 patients in order to evaluate the tolerability and the effects following the short-and long-term administration of this drug. The results of the large number of studies indicate that clodronate therapy does not have any clinically significant side-effects and confirm its tolerability and safety.

Bone Diseases↗
PubMed1991

Effect of propionyl carnitine on cardiac energy metabolism evaluated by the release of purine catabolites.

The assessment of purine release in perfusion fluid is a new method (Zucchi et al.) which allows a continuous evaluation of energy metabolism in isolated perfused rat heart. Purine release in fact is related to the imbalance between ATP formed and utilized in myocytes. With this method we have investigated the effect of propionyl carnitine, carnitine and propionate on the working heart. The presence of millimolar concentrations of propionyl carnitine decreases purine release and improves cardiac performance as measured by cardiac output and double product (product of heart rate and aortic systolic pressure). Propionate has no effect, while carnitine slightly decreases purine release. The property shown by propionyl carnitine in decreasing the imbalance between ATP production and utilization and in improving cardiac performance is due to its ability to improve the energy metabolism of cardiomyocytes. This compound supplies oxidizable substrates and intermediates to the tricarboxylic acid cycle. In the presence of propionyl carnitine the myocardium therefore responds better to the sudden requirements of overwork and shows better functional efficiency for longer periods.

Adenosine Triphosphate↗
PubMed1991

Effect of propionyl carnitine on energy charge and adenine nucleotide content of cardiac endothelial cells during hypoxia.

Adenine mucleotide metabolism is very active in endothelial cells. These cells are very rich in xanthine oxidase which may produce oxygen reactive species during ischaemia and reperfusion when a high amount of adenine nucleotides may be catabolized to hypoxanthine. We investigated the effect of propionyl carnitine on energy charge and nucleotide content in cultured endothelial cells during changes in oxygen partial pressure. During hypoxia the adenine nucleotide pool and the energy charge decreased more slowly in the presence of 0.5 mM propionyl carnitine than in the absence of the compound. Furthermore during reoxygenation a more rapid increase of energy charge and adenine nucleotide concentration was observed with propionyl carnitine. These observations suggest that the presence of propionyl carnitine allows the endothelial cells to maintain their functionality and regulatory role on vessel activity for a longer time and decreases the formation of oxygen reactive species due to xanthine oxidase activity on hypoxanthine formed by adenine nucleotide catabolism.

Adenine↗
PubMed1991

Protective effect of propionyl carnitine against peroxidative damage to arterial endothelium membranes.

Endothelial cells may be damaged by oxygen reactive species produced by granulocytes, by transition metal ions or by xanthine oxidase, an enzyme present in great quantity in these cells. Since it has been observed that propionyl carnitine protects the heart from peroxidation, we have investigated the effect of this compound on the formation of thiobarbituric acid reactive oxidation products (TBAR) in endothelial membranes. The peroxidation systems used were a mixture of Fe3+ and Fe2+, hydrogen peroxide and Fe2+, or xanthine oxidase-- xanthine. Propionyl carnitine at millimolar concentrations decreases TBAR formation. The protection is concentration-dependent and is almost absent in the presence of propionate and carnitine. From these results it appears that propionyl carnitine may protect not only myocardium but also vessels from peroxidative damage that occurs during ischaemia and reperfusion.

Animals↗
PubMed1990

Protective action of propionyl-L-carnitine on toxicity induced by hyperbaric oxygen.

The protective effect of propionyl-L-carnitine against hyperbaric oxygen toxicity was studied by in vivo experiments on mice. The treatment reduced both the percentage of animals with convulsions and the death rate. Tissue signs of toxicity and pulmonary weight increase were less marked in treated animals than in controls. Results may indicate that propionyl-L-carnitine needs to build up to critical levels in cells and mitochondria before its metabolic effects can be fully felt.

Animals↗
PubMed1990

Hyperbaric oxygen- and ethanol-induced infiltration of rat hepatic triglycerides and the protective action of coenzyme A.

The ethanol-induced increased synthesis of fatty acids in the liver is enhanced by hyperbaric oxygen exposure. Both lipid peroxidation and glutathione depletion are involved in these hepatic alterations. Coenzyme A can intervene in these mechanisms. The administration of CoA prevents hepatic lipid infiltration and the glutathione reduction induced in the rats by ethanol and hyperbaric oxygen exposure.

Animals↗