800 resultados para Microregión Zárate-Campana


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Four groups of 10 young adult Wistar male rats were fed ad libitum on a protein-free diet for periods of 7, 28, 56 and 84 days. Control groups were fed on a 20% casein diet. Food intake and body weights of rats were registered. Plasma protein levels and liver weight and fat content were determined. Sections of the caudate lobe were studied histologically. Fatty changes were classified in three grades. Protein-deficient rats exhibited loss of body weight and had low levels of plasma protein concentration. Liver lost weight after 7 days of protein deficiency; there was a gradual reduction in liver weight as periods of protein deprivation were longer. After 7 days, liver fat concentration was not significantly higher than in the respective control group; it was significantly higher in all the other malnourished animals, As periods of protein deprivation were longer, fatty changes became more severe. Other hepatic lesions were found in 5 of the 10 rats submitted to the longest period of protein deficiency. One of the rats showed a diffuse cellular atrophy, 2 animals showed an extensive haemorrhagic necrosis, another showed a focal area of reticulum collapse and the last exhibited a distortion of the normal architecture of the liver due to diffuse reticulum collapse and early nodular regeneration; these 2 last rats showed early fibrosis in portal areas. The findings suggest that other deficiencies may complicate the protein deficiency when rats are given a protein-free diet over prolonged periods. Even if the protein-deficient diet has protective nutrients, it may be that, when rats eat less food, as occurs in prolonged experiments deficiency of one or all of these elements can occur, depending on their relative amount in diet.

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An experiment was performed in order to evaluate the beta-glucuronidase activity in gastric juice and gastric mucosa of rats submitted to a protein-free diet. A group of 36 young adult male Wistar rats was fed a protein-free diet ad libitum for five weeks; a second group of 36 Wistar rats ingested a purified isocaloric 12,5% casein diet for the same period. The concentration of proteins in plasma, gastric juice and gastric glandular mucosa and the beta-glucuronidase activity in the gastric juice and gastric glandular mucosa were determined. Protein deficient rats had lower plasma protein concentrations and also lower protein concentrations in gastric juice and gastric mucosa. In these animals there was no significant change of beta-glucuronidase activity in the gastric juice, but there was a significant increase of the specific enzymatic activity in the gastric mucosa. The results suggest that protein restriction in young adult rats affects the gastric mucosa. The increase of the specific beta-glucuronidase activity might be due to heightened local catabolism or to a comparatively more severe protein depletion.

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To overcome the difficulties observed with fecal fat estimations, we studied fat absorption in 4 m to 12 years old children, assessing increments of serum triglycerides after administration of corn oil. Eighteen well-nourished children without gastrointestinal symptoms or parasites, 31 children with protein-calorie malnutrition (PCM), with or without protracted diarrhea and/or intestinal parasites and nine children with specific malabsorptive entities were studied. Serum triglycerides (TG) were measured before, 2 and 4 hours after the administration of 2 g/kg of corn oil per os. For control infants below 2 years no significant differences between the fasting level and those after 2 and 4 hours were observed. For children above this age significant absorption occurred by 2 hours but more intensively after 4 hours, an increment of TG above 35 mg% being considered normal. A good discrimination between TG increments of controls and malabsorptive children over 2 years was observed. In conclusion, the oral fat loading test, is applicable for children over 2 year of age. For infants below this age other schedules should be tested.

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The use of anthropometric measurements of triceps (TSF) and subscapular skinfolds (SSF) and mid-upper arm muscle circumference (MAMC) was examined as far as the diagnosis of energy-protein malnutrition (EPM) is concerned. The study was undertaken in five groups of patients (n = 231): arterial hypertension (AH, n = 63), chronic obstructive pulmonary disease (COPD, n = 17), hemodialyzed chronic renal failure (CRF, n = 19), critically ill patients with an acute event (CA, n = 42) and critically ill patients with chronic diseases (CCD, n = 90). The results were compared to those obtained in a group of healthy individuals (control group, n = 102). The control group and the group of patients were allocated in subgroups according to sex and age (less than 50 and more than 50 years). It was expected that significant differences would be found for the anthropometric values between the control subgroups and the COPD, the CRF and the CCD subgroups of patients. For the skinfold thicknesses (TSF and SSF), significant differences were found between CRF, CCD subgroups and the control subgroups under fifty years of age; however, the differences were not significant when the subgroups over fifty were analyzed. Concerning the MAMC, significant differences were found: 1 degree) between the CRF subgroups (males and females) and the control subgroups under fifty years of age; 2 degrees) between the CCD male subgroups (younger and older subgroups) and the respective control subgroups and 3 degrees) between the COPD and the control subgroups.(ABSTRACT TRUNCATED AT 250 WORDS)

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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In order to determine wheter blood gases abnormalities, specially hypoxemia, are associated with more marked changes in fat-free mass in patients with chronic obstructive pulmonary disease (CPOD), nutritional assessment was performed on 16 normoxemic (PaO 2 > 55 mm Hg) and 16 hypoxemic (PaO 2 < 55 mm Hg) COPD patients in stable clinical condition. Body weight was expressed as percentage of the ideal body weight. Fat-free mass was estimated by anthropometry (FFM-Anthr) and by bioelectrical impedance (FFM- BI). Handgrip-strength was assessed as a measure of peripheral skeletal muscle strength. Patients were age-matched and presented similar degree of airway obstruction. Malnutrition, defined as body weight less than 90% of the ideal, was observed in 19% of the normoxemic patients and in 25% of the hypoxemic patients (p>0,05). FFM values in hypoxemic patients, estimated by both methods, were not different from those observed in normoxemic patients. No significant difference was observed on handgrip values between the two groups. No correlation was found between nutritional indices and pulmonary function and gases exchange parameters. FFM correlated positively with values of peripheral muscle function in normoxemic and hypoxemic patients. These data add further evidence to the hypothesis that hypoxemia is not a primary cause of the nutritional deficiency observed in COPD patients.

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Patients with chronic heart failure (CHF) may develop a wasting syndrome, termed cardiac cachexia. This condition should be diagnosed when weight loss of more than 7.5% of the premorbid normal weight occurs over a time period of more than 6 months. Although the pathophysiologic causes of body wasting in patients with CHF remain unclear, studies have suggested that reduction of the dietary ingestion, intestinal malabsorption of nutrients, increased resting metabolic rates, and humoral neuroendocrine and immunologic abnormalities may play a role. The development of cachexia in the patients with CHF results in clinical symptoms, adverse consequences on the heart, and impaired survival.

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Tumour necrosis factor (TNF)-α has been found to be increased in malnourished chronic obstructive pulmonary disease (COPD) patients; however, the main cause of this phenomenon remains undetermined. In normal subjects, TNF-α production may be induced by dietary energy deprivation. The aim of this study was to investigate if stable COPD patients present alterations of inflammatory mediators after 48 h of dietary energy restriction. Fourteen COPD patients were admitted to the hospital while receiving an experimental diet with an energy content of approximately one-third of their energy needs. Clinical evaluation, nutritional assessment and serum levels of interleukin (IL)-6, TNF-α and C-reactive protein, and secretion of TNF-α by peripheral blood monocytes were assessed on admission and after the experimental diet. For reference values of the laboratory parameters, blood was collected from 10 healthy, elderly subjects. COPD patients showed significantly higher serum concentrations of IL-6 than control subjects, however, the experimental diet was not associated with statistically significant changes in the inflammatory mediators. The findings of this study, although preliminary because of the limited degree and duration of the energy restriction, suggest that the elevated levels of tumour necrosis factor-α, previously described in undernourished or weight-losing chronic obstructive pulmonary disease patients, may not be linked to a decrease of dietary energy intake.

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The aim of this study was to examine the agreement between the results of body fat (BF and BF%), fat-free mass (FFM) and FFM index (FFMI= FFM/height2) as estimated by skinfold anthropometry (ANT), bioelectrical impedance (BIA) and dual-energy X-ray absorptiometry (DXA) in two groups of men (> or = 50 y), one comprising healthy individuals (n=23) and the other, patients with chronic obstructive pulmonary disease (COPD) (n=24). Comparisons between body composition techniques were done by repeated measures ANOVA; the Bland & Altman procedure was used to analyse agreement. RESULTS AND CONCLUSIONS: 1) comparison between healthy and COPD groups showed significant differences between all studied variables; 2) in the healthy group, values for BF, BF%, FFM and FFMI were not significantly different when BIA or ANT was compared to DXA; however, in COPD, values for BF and BF% were significantly higher and for FFM and FFMI significantly lower when BIA was compared to DXA; in contrast, no differences were shown between values for these variables when ANT was compared with DXA; 3) Bland & Altman test, in both groups, showed no agreement between BIA and DXA and between ANT and DXA; it was also shown that body fat was overestimated and fat free mass underestimated by BIA in relation to DXA.

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The objective of this study was to investigate the effects of exposure to tobacco smoke (ETS) in rats that were or were not supplemented with dietary β-carotene (BC), on ventricular remodeling and survival after myocardial infarction (Ml). Rats (n = 189) were allocated to 4 groups: the control group, n = 45; group BC administered 500 mg/kg diet, n = 49, BC supplemented rats; group ETS, n - 55, rats exposed to tobacco smoke; and group BC+ETS, n = 40. Wistar rats weighing 10O g were administered one of the treatments until they weighed 200 to 250 g (∼5 wk). The ETS rats were exposed to cigarette smoke for 30 min 4 times/d, in a chamber connected to a smoking device. After reaching a weight of 200-250 g, rats were subjected to experimental MI (coronary artery occlusion) and mortality rates were determined over the next 105 d. In addition, echocardiographic, isolated heart, morphometrical, and biochemical studies were performed. Mortality data were tested using Kaplan-Meyer curves and other data by 2-way ANOVA. Survival rates were greater in the ETS group (58.2%) than in the control (33.3%) (P = 0.001) and BC+ETS rats (30.0%) (P = 0.007). The groups did not differ in the other comparisons. Left ventricular end-diastolic diameter normalized to body weight was greater and maximal systolic pressures were lower in the ETS groups than in non-ETS groups. Previous exposure to tobacco smoke induced a process of cardiac remodeling after MI. There is a paradoxical protector effect with tobacco smoke exposure, characterized by lower mortality, which is offset by BC supplementation. © 2005 American Society for Nutritional Sciences.

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The objective of this study was to evaluate the role of retinoic acid in experimental postinfarction myocardial remodeling. Wistar rats were subjected to myocardial infarction (MI) and treated with retinoic acid (RA), 0.3 mg/(kg · d) (MI-RA, n = 29), or fed a control diet (MI, n = 34). After 6 mo, the surviving rats (MI-RA = 18 and MI = 22) underwent echocardiograms, and isolated hearts were tested for function in vitro. The cross-sectional area of the myocyte (CSA) and interstitial collagen fraction (IC) were measured in a cross section of the heart stained by hematoxylin-eosin and picrosirius red, respectively. The CSA was smaller in the MI-RA group [229 (220, 234) μm 2] [medians (lower quartile, upper quartile)] than in the MI group [238 (232, 241) μm 2] (P = 0.01) and IC was smaller in the MI-RA group [2.4 (1.7, 3.1)%] than in the MI group [3.5 (2.6, 3.9)%] (P = 0.05). The infarct size did not differ between the groups [MI = 44.6 (40.8, 48.4)%, MI-RA = 45 (38.6, 47.2)%]. Maximum rate of rise of left ventricular pressure (+dp/dt) was greater in the MI-RA group (2645 ± 886 mm Hg/s) than in the MI group (2081 ± 617 mm Hg/s) (P = 0.05). The other variables tested did not differ between groups. Retinoic acid supplementation of rats for 6 mo attenuates the ventricular remodeling process after MI. © 2005 American Society for Nutrition.

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Objective: We studied the effects of β-carotene (BC) on ventricular remodeling after myocardial infarction. Methods: Myocardial infarction was induced in Wistar rats that were then treated with a BC diet (500 mg/kg of diet per day; MI-BC; n = 27) or a regular diet (MI; n = 27). Hearts were analyzed in vivo and in vitro after 6 mo. Results: BC caused decreased left ventricular wall thickness (MI = 1.49 ± 0.3 mm, MI-BC = 1.23 ± 0.2 mm, P = 0.027) and increased diastolic (MI = 0.83 ± 0.15 cm2, MI-BC = 0.98 ± 0.14 cm2, P = 0.020) and systolic (MI = 0.56 ± 0.12 cm2, MI-BC = 0.75 ± 0.13 cm2, P = 0.002) left ventricular chamber areas. With respect to systolic function, the BC group presented less change in fractional area than did controls (MI = 32.35 ± 6.67, MI-BC = 23.77 ± 6.06, P = 0.004). There was no difference in transmitral diastolic flow velocities between groups. In vitro results showed decreased maximal isovolumetric systolic pressure (MI = 125.5 ± 24.1 mmHg, MI-BC = 95.2 ± 28.4 mmHg, P = 0.019) and increased interstitial myocardial collagen concentration (MI = 3.3 ± 1.2%, MI-BC = 5.8 ± 1.7%, P = 0.004) in BC-treated animals. Infarct sizes were similar between groups (MI = 45.0 ± 6.6%, MI-BC = 48.0 ± 5.8%, P = 0.246). Conclusion: Taken together, these data suggest that BC has adverse effects on ventricular remodeling after myocardial infarction. © 2006 Elsevier Inc. All rights reserved.

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Background: The role of the adrenergic system on ventricular remodeling induced by cigarette smoking is unknown. Objective: To investigate the influence of propranolol on ventricular remodeling induced by exposure to tobacco smoke. Methods: Rats were divided into three groups: 1) C, n=10 - control group; 2) F, n=10 - animals exposed to tobacco smoke; 3) BB, n=10 - animals receiving propranolol and exposed to tobacco smoke (40 mg/kg/day). After 2 months, the animals underwent echocardiographic and morphometric analyses. One-way ANOVA (mean ± standard deviation) or the Kruskal-Wallis test (median and interquartile interval) was used. Results: Group BB showed a lower heart rate than group F (C = 358 ± 74 bpm, F = 374 ± 53 bpm, BB = 297± 30; P = 0.02). Group F showed greater end-diastolic diameters (C = 18.6 ± 3.4 mm/kg, F = 22.8 ± 1.8 mm/kg, BB = 21.7 ± 1.8 mm/kg; P = 0.003) and left ventricular (LV) end-systolic diameters (C = 8.6 ± 2.1 mm/kg, F = 11.3 ± 1.3 mm/kg, BB = 9.9 ± 1.2 mm/kg; P = 0.004), adjusted for body weight (BW) and a tendency towards a lower ejection fraction (C = 0.90 ± 0.03, F = 0.87 ± 0.03, BB =0.90 ± 0.02; P = 0.07) than group C. Group BB showed a tendency towards a lower LV/BW ratio than group F (C = 1.94 (1.87 - 1.97), F = 2.03 (1.9-2.1) mg/g, BB = 1.89 (1.86-1.94); P = 0.09). Conclusion: Administration of propranolol attenuated some of the variables of ventricular remodeling induced by the exposure to tobacco smoke in rats.

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Background: To investigate the effect of lisinopril on cardiac remodeling induced by smoking. Material/Methods: Rats were allocated into 3 groups: group CON (n=8): control; group CSE (n=8): cigarette smoke exposure; group CSE-LIS (n=8): exposed to tobacco smoke and treated with lisinopril. Results: After 2 months, the tail systolic pressure was lower in CSE-LIS (CON=116 ±27 mm Hg, CSE=126±16, CSE-LIS=89±12; P<.001). CSE animals showed higher left ventricular systolic diameter (CON=8.25±2.16 mm/kg, CSE=11.5±1.3, CSE-LIS=9.27±2.00; P=.009) and myocyte cross-sectional area (CON=245±8 μm2, CSE=260±17, CSE-LIS=238±12; P=.01) than CON and CSE-LIS. The ejection fraction (CON =0.91±0.02, CSE=0.86±0.02, CSE-LIS=0.92±0.03; P=.002) and fractional shortening (CON=55.7±4.41%, CSE=48.7±3.43, CSE-LI=58.2±7.63; P=.006) were lower in CSE group than CON and CSE-LIS. CSE and CSE-LIS animals showed higher collagen amounts (CON=3.49±0.95%, CSE= 5.01±1.58, CSE-LIS=5.27±0.62; P=.009) than CON. CON group showed a higher connexin 43 amount in the intercalated disc (CON=3.70±0.38, CSE=2.13±0.53; CSE-LIS=2.17±0.73; P=.004) than CSE and CSE-LIS. There were no differences in IFN-g or TNF-a cardiac levels among the groups. Conclusions: Lisinopril attenuated both morphologic and functional abnormalities induced by exposure to tobacco smoke. In addition, this effect was associated with diminished blood pressure, but not alterations in connexin 43 distribution, cytokine production or collagen amount. © Med Sci Monit, 2010.