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Biomedical subjects

S Zucoloto

Publications and source records attributed to S Zucoloto.

At least 73 records · Page 4Linked to original sources
PubMed1980

Effect of protein-calorie malnutrition on catecholamine levels and weight of heart in rats.

Catecholamine levels and weight of heart were studied in rats subjected to protein-calorie malnutrition and after a period of nutritional rehabilitation. Rats given a protein deficient diet (4% protein) for periods of 6 and 12 weeks showed a severe restriction of body weight gain. Nevertheless, even though the measured heart weight of deficient rats was significantly lower than the respective controls (16% protein), the deficient rats incurred "real" cardiac enlargement since the mean heart weight of the equal body weight controls was significantly different from that of the deficient animals. The mean heart weight of rats fed a high-protein diet for 6 weeks thereupon a 6-week period of protein deprivation was still less than that of controls, and the heart ratio was still greater than that of controls. However, the heart weight of rehabilitated rats was not significantly different from that of equal body weight controls. Serum protein and albumin levels in dificient rats were significantly decreased in comparison to rats fed a high-protein diet. While the serum protein levels of rehabilitated rats were lower than those of controls, the albumin levels were not different. The protein-calorie malnourished rats, which received a low-protein diet for 6 and 12 weeks, showed a significant increase in myocardium noradrenaline concentration. After a period of nutritional rehabilitation this change did not persist. These catecholaminergic alterations in heart may be responsible, at least in part, for the different cardiac abnormalities described as a result of protein-calorie dietary deficiency. It may also explain the "real" cardiac enlargement observed in deficient rats, according to the hypothesis that noradrenaline may be the ultimate myocardial hypertrophy hormone.

Animals↗
PubMed1980

Impairment of fat absorption induced by alcohol in rats.

Rats were maintained 16 weeks on a well-balanced semipurified solid diet supplemented with alcohol which comprised 35% of total calories. A control group was pair-fed the same basic diet with sucrose replacing alcohol isocalorically. Fecal fat excretion was evaluated. The mean fecal fat excretion of alcohol-fed rats was 40% higher than that of pair-fed controls. The possible pathogenic mechanism of such functional alteration is discussed.

Animals↗
PubMed1979

Effect of chronic ethanol consumption on mucosal morphology and mitotic index in the rat small intestine.

Rats were maintained 16 weeks on a well-balanced semisynthetic solid diet supplemented with ethanol which comprised 35% of total calories. A control group was pair-fed the same basic diet with sucrose replacing ethanol isocalorically. Striking changes in mucosal morphology and mitotic index were observed in the jejunum and ileum of ethanol-fed rats in comparison to pair-fed controls. Furthermore, it is significant that these changes were more pronounced in the ileum than in the jejunum. Since ethanol is almost completely absorbed in the stomach and upper intestine, under the conditions of this study, we propose that, apart from a possible topical toxic effect of ethanol, there appear to be other separate possible causes of the extensive small intestinal changes found in ethanol-fed rats. The first is that the changes are due to injurious effects of blood-borne ethanol; secondly, the changes could be a functional adaptation due to altered luminal nutrition as a consequence of the introduction of ethanol in the diet.

Alcoholism↗
PubMed1978

Hepatic damage produced by long-term alcohol consumption in well-nourished rats.

A study of the effect of long-term alcohol consumption on the liver of well-nourished rats is described. Rats fed for 16 weeks on a semipurified diet supplemented with high levels of vitamins and lipotropic factors and alcohol corresponding to 35% of the total caloric intake developed marked fatty changes of the liver. Mild fatty changes were observed in pair-fed controls receiving as isoenergetic equivalent of sucrose instead of alcohol. Intracellular hyaline bodies, corresponding ultrastructurally to giant mitochondria were abundantly found in the hepatocytes of alcoholic rats, while in the controls they were not seen. Te findings in this investigation are postulated to provide further evidence that the long-term intake of alcohol exerts a direct causative role in the pathogenesis of liver damage.

Alcoholism↗
PubMed1978

Condition of rat testes after prolonged ethanol consumption.

Rats were maintained 16 weeks on a well-balanced, semisynthetic, solid diet supplemented with ethanol, which comprised 35% of total calories. A control group was pair-fed the same basic diet with sucrose replacing ethanol isocalorically. On light microscopy, the ethanol-fed rats showed appreciable fatty changes in the liver, while the controls did not. There were no differences in testicular morphology between ethanol-fed and control rats, both of which appeared to be normal. The present findings support the view that ethanol is directly toxic to the liver, but under the present experimental conditions, not directly toxic to the testes.

Alcoholism↗
PubMed1977

Effect of chronic ethanol ingestion on the small intestinal ultrastructure in rats.

Rats maintained for a period of 16 weeks on a supplemented solid semisynthetic diet and ethanol corresponding to 35% of the total caloric intake developed ultrastructural changes in the small intestine as compared to pair-fed controls. The enterocytes from jejunal and ileal villi of the alcoholic animals exhibited conspicuous alterations of mitochondria and smooth and rough endoplasmic reticulum. The mitochondrial changes were characterized by enlargement, swelling, decreased matrical density, ruptured cristae, and occasional myelin figures. The smooth endoplasmic reticulum was dilated and apparently proliferated in a few epithelial cells. The rough endoplasmic reticulum appeared scarce with fewer ribosomes attached to the cisternae. These findings are postulated to provide further evidence that the chronic consumption of ethanol exerts a direct causative role in the pathogenesis of small intestinal damage in rats. Furthermore it can be especulated that these changes could be responsible, at least in part, for the functional abnormalities commonly found in chronic alcoholism.

Alcoholism↗
PubMed1976

Heart norepinephrine concentration after chronic alcohol ingestion in the rat.

The effect of long-term alcohol ingestion on the norepinephrine concentration of the heart was investigated in rats. The alcoholic animals showed a highly significant increase in cardiac norepinephrine concentration as compared with the corresponding controls. It is further suggested that continued exposure to high levels of norepinephrine may play a role in the development of cardiomyopathy in chronic alcoholism.

Alcoholism↗
PubMed1976

[Norepinephrine levels and morphologic alterations of myocardium in chronic alcoholic rats].

Experimental alcoholism was produced in rats by giving them 32% alcohol as the only source of liquid for 4, 12, and 24 weeks. Control rats were given no alcohol. After 12 and 24 weeks on test the alcohol-fed animals developed pathologic changes and tissue catecholamine alterations of the myocardium. However after 4 weeks there were no differences in myocardial structure and norepinephrine levels between alcohol-fed and control rats. The present experiments indicate that marked increase in norepheinephrine concentration accompanies morphologic evidence of myocardial degeneration and may play a role in the development of the alcoholic cardiomyopathy.

Alcoholism↗
PubMed1975

[Stress due to immobilization and low protein intake in rats. Biochemical changes].

Rats fed a control casein diet, when exposed to immobilization, loose more nitrogen, urea and vitamin C in urine. Animals receiving a protein deficient diet excrete less nitrogen, urea and ascorbic acid in urine than their controls. When protein deficiency and immobilization are associated, there is not an increase on the urinary excretion of those substance compared to the deficient animals.

Animals↗
PubMed1975

[Stress caused by immobilization and low protein intake in rats. Morphological changes].

The periodic immobilization of the animals receiving a control diet resulted in a smaller weight gain than in controls. The animals fed a protein deficient diet gained also less weight as compared to controls. The association of the deficiency and the stress of immobilization further decreases the weight gain, but the differences were not significant. The animals submitted to restraint or protein deficiency stress showed an increase in their heart weight in relation to body weight. This increase in more significant when immobilization and protein deficiency were associated. The degree of cardiac muscle fibers damage was also found more pronounced in this group of animals, when analysed through histochemical methods. Liver weight was not found different in the animals submitted to the experimental program. Histological examination of this organ showed fatty infiltration in the protein deficient animals. The picture was not found to be agravated when the animals were further stimulated by the restraint mechanism. Spleen weight was found to be similar in all groups. Histological study of the protein deficient group showed small lesions, that were increased when the deficiency was associated to immobilization. The relative testis weight of the restraint animals receiving the control diet was found to be similar to the animals not immobilized. The protein deficient animals have significantly smaller testis weight than the well nourished group. The histologic study showed that restraint or protein deficiency are responsible for a sexually retarded animal, but the lesions increased with the association of restraint and deficiency.

Animals↗
PubMedDate not supplied

Therapeutic effect of hyperbaric oxygen in hepatic artery thrombosis and functional cholestasis after orthotopic liver transplantation.

Among the postoperative complications, hepatic artery thrombosis can occur in up to 10% of adult orthotopic liver transplants and intervention is indicated when this occurs within 30 days by retransplantation. Primary graft dysfunction, which can occur in up to 30% of the cases and is another potential complication, although reversible, has a relatively high mortality rate. Hyperbaric therapy, an efficient mode of tissue oxygenation, is being used in an increasing number of clinical situations. We report here two cases where hyperbaric oxygen therapy greatly benefited patients with complications after orthotopic liver transplantation: one with hepatic artery thrombosis and the other with primary graft dysfunction. Both patients showed rapid clinical recovery with gradual reduction of liver and canalicular enzymes soon after commencing hyperbaric oxygen therapy.

Adult↗
PubMedDate not supplied

Effect of hyperbaric oxygen on liver regeneration in a rat model.

Hyperbaric oxygen therapy is a treatment that has been gradually implemented for the treatment of several pathologic conditions. The present study evaluated the effect of hyperbaric oxygen therapy for hepatic regeneration and its relationship to mitochondrial function. Male Wistar rats underwent partial hepatectomy (70%) and subsequently underwent two sessions of hyperbaric oxygen (90 minutes each, at a pressure of 2 ATA). The animals were sacrificed at 24 and 48 hours after surgery. Hepatic regeneration was evaluated by the dry weight of the remaining liver, the hepatic regeneration rate, the hepatic DNA content, and the hepatocyte proliferation rate using the "proliferating cell nuclear antigen" (PCNA) content. Function of the mitochondria was evaluated by its oxygen consumption during respiratory states 3 and 4, its respiratory control ratio (RCR), its membrane potential, as well as its osmotic swelling. We also measured serum levels of aminotransferases. The results revealed an increased dry weight of the remaining liver, regeneration rate, and DNA content at 24 and 48 hours after hepatectomy. The hepatocyte proliferation rate was significantly higher among animals treated with hyperbaric oxygen therapy at 48 hours after surgery. There was no significant difference in aminotransferase levels. Mitochondrial respiration revealed reduced oxygen consumption in state 3 after 48 hours. These results demonstrated that hyperbaric oxygen stimulates hepatic regeneration at 24 and 48 hours after 70% hepatectomy. The effect of hyperbaric oxygen on hepatic tissue occurs without tissue damage and protects mitochondria after 48 hours.

Alanine Transaminase↗
PubMedDate not supplied

The differential regulation of human telomerase reverse transcriptase and vascular endothelial growth factor may contribute to the clinically more aggressive behavior of p63-positive breast carcinomas.

p63, a p53 homologue, is a myoepithelial cell marker in the normal mammary gland but p63-positive neoplastic cells may be found in up to 11% of invasive breast carcinomas. This study aims to verify the relationship between p63 expression and several clinicopathological features and tumor markers of clinical significance in breast pathology including key regulators of the cell cycle, oncogenes, apoptosis-related proteins, metalloproteinases and their inhibitors. Immunohistochemistry with 27 primary antibodies was performed in 100 formalin-fixed paraffin-embedded samples of invasive ductal carcinomas. p63-positive cells were found in 16% of carcinomas. p63-positive carcinomas were poorly differentiated, hormone receptor-negative neoplasms with a high proliferation rate. p63 also correlated with advanced pathological stage, tumor size, and the expression of human telomerase reverse transcriptase (hTERT), tissue inhibitor of matrix metalloproteinase 1 (TIMP1) and vascular endothelial growth factor (VEGF). The expression of TIMP1 suggests that the anti-proteolytic stimuli may be preponderant in p63-positive carcinomas. hTERT activity is associated with nodal metastases and cellular proliferation. VEGF regulates angiogenesis, which is also a fundamental event in the process of tumor growth and metastatic dissemination. Thus, the differential regulation of hTERT and VEGF in p63-positive breast carcinomas may contribute to the clinically more aggressive behavior of these neoplasms.

Adult↗