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Biomedical subjects

M A Rossi

Publications and source records attributed to M A Rossi.

At least 91 records · Page 5Linked to original sources
PubMed1989

Electron-microscopic study of systemic myonecrosis due to poisoning by tropical rattlesnake (Crotalus durissus terrificus) in humans.

This article describes the ultrastructural study of skeletal muscle biopsy specimens from five patients following envenomization by tropical rattlesnake (Crotalus durissus terrificus). All the patients were bitten in the leg and the biopsy specimens were obtained from the contralateral gastrocnemius muscle in the middle of the lower leg. A wide spectrum of detailed ultrastructural changes involving muscle fibers and microvasculature was demonstrated. Essentially, such lesions included widespread necrotic myofibers intermixed with intact fibers, accompanied by changes in the endothelial lining of the intramuscular blood capillaries and small arterial vessels, reducing their lumens. Since these alterations were observed in biopsy specimens from the limb contralateral to the site of the bite, they clearly demonstrate the systemic myonecrotic action of the venom of a tropical rattlesnake. On the basis of these data, the mechanism of venom-induced myopathy is described. It is postulated that the pathogenesis of systemic myonecrosis due to poisoning by C durissus terrificus is a complex one, probably due to direct damage to cells by the myotoxins of the venom, as well as indirect effects due to ischemia.

Adolescent↗
PubMed1988

Analysis of glutathione-dependent enzyme activities in two different rat hepatomas and in normal liver in relation to their role in resistance to oxidative stress.

The importance of some glutathione metabolic pathways was examined in two highly dedifferentiated hepatomas, Yoshida AH-130 and Morris 3924 A hepatomas, and in normal liver in relation to their role against oxidative stress. The cytosol prepared from Yoshida hepatoma cells decreased the peroxidation rate in normal liver microsomes and mitochondria, but this antioxidant property was not displayed by Morris hepatoma. Glutathione peroxidase and glutathione-S-transferases activities were extremely low in both hepatomas; glutathione reductase activity values were about half the normal liver values. The large decrease in glutathione peroxidase and glutathione-S-transferases suggests that in these two tumors only small amounts of GSH can be used in reduction or conjugation reactions, such as the reduction of hydrogen peroxide and lipid hydroperoxides or the conjugation of GSH with the end products of lipoperoxidation, aldehydes or ketones. The hypothesis of a more efficient GSSG reduction in hepatomas, due to the low glutathione peroxidase/glutathione reductase activity ratio, is also discussed. The described changes in glutathione related enzymes do not seem to have any correlation with the protective effect against the lipoperoxidative processes displayed by some tumors since these enzymatic activities were similar in both hepatomas whereas only Yoshida hepatoma showed antioxidant properties.

Animals↗
PubMed1988

Stimulation of phospholipase C activity by 4-hydroxynonenal; influence of GTP and calcium concentration.

4-Hydroxynonenal (HNE), a major aldehyde end-product of lipid peroxidation, induces in vitro a rapid stimulation of rat liver PIP2-phospholipase C. At physiological Ca2+ concentration the effect of the aldehyde is strongly potentiated by guanosine thiotriphosphate (GTP gamma S); GPT gamma S; at higher Ca2+ levels the acceleration of PIP2 breakdown induced by the aldehyde reaches very high values, but is no longer modulated by the presence of GTP gamma S. As the concentration of the aldehyde used (1 micromolar) can be actually reached in tissues, the effects shown in vitro are likely to occur in vivo.

Aldehydes↗
PubMed1987

Immune complex glomerulonephritis in experimental kala-azar.

In the present work we demonstrate that hamsters infected with L. donovani eliminate large quantities of immunoglobulins in the urine. This alteration is clearly a consequence of a conspicuous immune complex glomerulonephritis readily detectable 7 days after the beginning of infection. L. donovani antigens and hamsters immunoglobulins (Igs) were revealed as granular deposits in the mesangial areas and contiguous loops of the glomeruli. Histopathological alterations such as focal mesangial proliferation with progression to diffuse proliferation were observed in the first 3 weeks of infection. From day 35 onwards, all diseased animals presented large deposits of amyloid material of predominantly glomerular localization. In consonance with these alterations, Igs were detected in the urine by day 21 of infection and their concentration increased substantially with the progression of disease. In contrast, serum Igs increased until day 21, when their concentration dropped steadily.

Amyloid↗
PubMed1987

Drug-induced left ventricular failure in patients with pulmonary disease. Endomyocardial biopsy demonstration of catecholamine myocarditis.

Three patients with severe chronic lung disease had left ventricular failure develop with marked impairment of cardiac function. Ejection fractions by radioactive blood pool ventriculography were 0.17, 0.24, and 0.20. Right ventricular endomyocardial biopsy specimens showed interstitial hemorrhage and foci of interstitial polymorphonuclear leukocytes, strongly suggestive of catecholamine myocarditis. These patients had used beta-adrenergic agonist inhalants and methylxanthines. One of them clearly abused the inhalant and had elevated levels of urinary catecholamines. Progressive deterioration of pulmonary and cardiac function occurred in two patients, with death within three months of the initial myocardial biopsy. Concomitant use of beta-adrenergic agonists and methylxanthines may cause myocarditis with left ventricular failure in susceptible patients.

Adrenergic beta-Agonists↗
PubMed1986

The evolution of experimental Trypanosoma cruzi cardiomyopathy in rabbits: further parasitological, morphological and functional studies.

Young rabbits (1-2 months of age) inoculated with trypomastigote forms of the Colombia strain of Trypanosoma cruzi have been shown to develop cardiac pathological changes (together with parasitological and immunological alterations) which are very similar to those observed in the acute and chronic phases of Chagas' disease in man. The cardiac alterations in the acute phase are characterized grossly by slight cardiomegaly with dilatation of the right-sided chambers. Microscopically they are characterized by mild focal myocarditis. The chronic phase is characterized by moderate to marked cardiomegaly with hypertrophy and dilatation of both ventricular chambers. There is thinning of the apical region (apical aneurysm), particularly of the left ventricle. Focal myocarditis is seen microscopically with areas of myocytolytic necrosis, atrophic and hypertrophic myofibers, an inflammatory response predominantly composed of mononuclear cells and interstitial fibrosis. Cineventriculography in the left ventricle of rabbits during the chronic phase disclosed regional myocardial dysfunction, with typical apical systolic bulging. The pathogenesis of Chagasic cardiomyopathy is briefly discussed in the light of these findings. Our investigation has further shown that this animal model is particularly suitable for studies on on the mechanisms, pathology and treatment of Chagas' heart disease.

Actin Cytoskeleton↗
PubMed1986

Calcific degeneration of pericardial valvular xenografts implanted subcutaneously in rats.

Tissue valve dystrophic calcification, resulting in hemodynamic regurgitation and/or stenosis, is the most serious complication when bioprosthetic heart valves are concerned. The objective of this investigation was to define morphologically the sequential development of calcific deposits in pericardial tissue cusps of unimplanted cardiac bioprostheses implanted subcutaneously in rats. Small samples of pericardium were implanted subcutaneously in the dorsal area of young rats weighing 60-80 g. The animals were selected randomly and sacrificed at days 1, 2, 7, 14 and 28 after implantation. The specimens were retrieved and studied morphologically. Calcific deposits were seen grossly as small punctate white masses from day 7 after implantation, progressively becoming more extensive. The light and electron microscopic studies showed that: calcific deposits occurred as early as 24 hours after implantation, the calcific degenerative process was progressive with time, and the mineralization was diffuse, although irregular in degree. The ultrastructural findings revealed that cytoplasmic organelles (mitochondria in particular) and plasma membrane of connective tissue cells appear to serve as initial sites of the process of calcification, which then progresses in the interfibrillar spaces, adjacent to collagen fibrils and elastic fibers.

Animals↗
PubMed1986

New data on kinetics of lipid peroxidation in experimental hepatomas and preneoplastic nodules.

Lipid peroxidation has been found decreased in several hepatomas. The decline has been shown already at the level of preneoplastic nodules obtained after DEN treatment of rats. A substantial exception is represented by the hepatoma cell line MH1C1, deriving from a slightly deviated Morris tumor. Most of the described experiments estimated lipid peroxidation levels in terms of malonaldehyde production by the thiobarbituric acid test. It is now clear that this test does not account for several other aldehydes produced during lipid peroxidation. We now investigated by high performance liquid chromatography (HPLC) the whole range of non-polar aldehydes produced by tumor homogenates and by preneoplastic nodules both in basal conditions and after stimulation with ADP-iron or ascorbate. It was reduced in the preneoplastic nodules as well as in the DEN-induced hepatoma. The susceptibility to the prooxidant effect of ADP-iron or ascorbate was strongly decreased in all hepatomas as well as in preneoplastic nodules. It has been recently published that hepatoma cells are more susceptible than normal liver to the toxic action of aldehydes. This was attributed at least in part to the decreased activity of aldehyde dehydrogenases, as well as to their different distribution in tumor cells. A deeper study on aldehyde metabolism in hepatomas has shown that alcohol dehydrogenase and NADPH-aldehyde reductase also are markedly decreased in Yoshida hepatoma cells and the MH1C1 cell line. However, glutathione transferase, that can use hydroxynonenal as a substrate, is strongly decreased in Yoshida hepatoma cells but not in MH1C1 cells.

Alcohol Dehydrogenase↗
PubMed1986

Glutathione synthesis in normal liver and in Yoshida AH-130 hepatoma.

The amount of reduced glutathione in transplantable hepatomas and in a primary DEN-induced hepatoma is lower than in normal liver. In all tumors examined, the glutathione decrease is not due to an increase of oxidized glutathione. In this paper the in vitro activities of two enzymes involved in glutathione synthesis, gamma-glutamylcysteine synthetase and glutathione synthetase, are studied in normal adult rat liver, in regenerating rat liver and in highly anaplastic Yoshida AH-130 hepatoma cells. The activity of these enzymes was determined in the postmicrosomal supernatant fraction as nmoles of [U-14C]-glutamate incorporated into product per mg of soluble protein. In Yoshida AH-130 hepatoma, the gamma-glutamylcysteine synthetase and glutathione synthetase activities are lower in respect to normal liver. This is in agreement with the low glutathione content observed in the hepatoma cells. On the other hand, in regenerating liver, there are minimal differences in comparison with normal liver.

Animals↗
PubMed1985

Nephropathy produced by Forssman antibody in guinea pigs: an experimental model of mesangial injury.

In the present work the involvement of the kidneys of guinea pigs injected with rabbit anti-sheep red blood cell antiserum (Forssman antibody) was studied. The antibody was introduced by a catheter into the abdominal aorta close to the openings of renal arteries. Glomerular lesions were observed 6 h following the injection: increased cellularity at the expense of polymorphonuclear and mononuclear cells, widened mesangial regions, deposits of fuchsinophilic material in the mesangium and capillary loops. By immunofluorescence the antibody was detected in the mesangial region extending to adjacent capillary loops, but it was not possible to demonstrate the presence of complement with certainty. The presence of subepithelial nodules on the glomerular basement membrane and deposits in the mesangium was demonstrated by electron microscopy. These findings suggest that this glomerulopathy induced by Forssman antibody may be a simple and reproducible model for the study of mesangial lesions.

Animals↗
PubMed1985

Myonecrosis, myoglobinuria and acute renal failure induced by South American rattlesnake (Crotalus durissus terrificus) envenomation in Brazil.

The venom of the Brazilian rattlesnake Crotalus durissus terrificus is know to have hemolytic and neurotoxic physiopathological activities which may cause acute renal failure with hemoglobinuria and/or methemoglobinuria. As far as we know, no report has been published on the ability of the venom of this rattlesnake species to cause rhabdomyolysis. In the present paper we demonstrate that the venom of Brazilian snakes of the genus Crotalus can induce systemic myonecrosis. Clinical, laboratory and anatomo-pathological data for two patients referred to the University Hospital of the Faculty of Medicine of Ribeirão Preto, University of São Paulo, 24 hr after a rattlesnake bite, are presented. In both cases, exaggerated elevation of serum levels of the enzymes creatine phosphokinase, lactate dehydrogenase and glutamic-oxaloacetic transaminase were detected, as well as data suggesting acute hypercatabolic renal failure. Immunoelectrophoresis of the serum and urine of these patients, carried out against specific anti-myoglobin serum (Behringwerke), demonstrated myoglobinemia and myoglobinuria, confirming injury to muscle tissue. Electron microscopy of a calf muscle biopsy taken from the leg contralateral to the bite from one patient revealed foci of myonecrosis.

Acute Kidney Injury↗