131 resultados para OLD RATS


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This work examined the histological effects, on the rat palatal mucosa, of a denture base acrylic resin, submitted or not to a post-polymerization heat-treatment. Methods: Fifteen adult female Wistar rats, with sixty days old, weighting 150 g – 250 g were divided in G1: animals being maintained under the same conditions as the experimental groups following described, but without the use acrylic palatal plates (control group); G2: use of heat-polymerized acrylic resin palatal plates made of Lucitone 550; G3: use of palatal plates identical to G2, but subjected to a post-polymerization treatment in a water bath at 55°C for 60 min. The plates covered all the palate and were fixed in the molar region with light-cured resin, thus being kept there for 14 days. After the sacrifice, the palate was removed, fixed in formaldehyde 10% and decalcified with EDTA. Sections were stained using haematoxylin and eosin. Images in duplicate were made from the central region of the cuts, to measure the thickness (μm) of the keratin layers (TKC), epithelium total (TET) and connective tissue (TCC). Statistical analyses were carried out by one-way ANOVA and Tukey post-tests (α=0.05). Results: According to the results there was significant difference in the thickness of keratin between G2 and G3, with G1 having the intermediate value and similar to the other groups. There was a significant difference in the connective tissue with G3

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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

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

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

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In renovascular hypertensive rats, low doses of angiotensin converting enzyme (ACE) inhibitors have been found to prevent myocardial hypertrophy independent of blood pressure level. This finding would suggest humoral rather than mechanical control of myocyte growth. The aim of this study was to examine the effect of nonantihypertensive doses of ACE inhibitor on myocardial hypertrophy and necrosis in hypertensive rats. Renovascular hypertension (RHT) was induced in four-week-old Wistar rats. Twenty-eight animals were treated for four weeks with three doses of ramipril (0.01, 0.1 or 1. 0 mg/kg/day, which are unable to lower blood pressure. Fourteen animals were not treated (RHT group). A sham operated, age/sex-matched group was used as control (n = 10). Myocardial histology was analysed in 3 microm thick sections of the ventricle stained with either haematoxylin-eosin, reticulin silver stain or Masson's trichrome. There was a significant correlation between systolic blood pressure and left ventricular to body weight ratio in both sets of animals: untreated plus controls and ramipril-treated rats. ACE inhibition prevented myocyte and perivascular necrosis and fibrosis in a dose-dependent manner. We conclude that myocardial hypertrophy in rats with renovascular hypertension is directly related to arterial pressure, and that this relationship is not affected by nonantihypertensive doses of ACE inhibitor. Myocardial necrosis/fibrosis and coronary artery damage induced by angiotensin II are prevented by ACE inhibitor in a dose-dependent manner, despite the presence of arterial hypertension.

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The aging spontaneously hypertensive rat (SHR) is a model in which the transition from chronic stable left ventricular hypertrophy to overt heart failure can be observed. Although the mechanisms for impaired function in hypertrophied and failing cardiac muscle from the SHR have been studied, none accounts fully for the myocardial contractile abnormalities. The cardiac cytoskeleton has been implicated as a possible cause for myocardial dysfunction. If an increase in microtubules contributes to dysfunction, then myocardial microtubule disruption by colchicine should promote an improvement in cardiac performance. We studied the active and passive properties of isolated left ventricular papillary muscles from 18- to 24-month-old SHR with evidence of heart failure (SHR-F, n=6), age-matched SHR without heart failure (SHR-NF, n=6), and age-matched normotensive Wistar-Kyoto rats (WKY, n=5). Mechanical parameters were analyzed before and up to 90 minutes after the addition of colchicine (10(-5), 10(-4), and 10(-3) mol/L). In the baseline state, active tension (AT) developed by papillary muscles from the WKY group was greater than for SHR-NF and SHR-F groups (WKY 5.69+/-1.47 g/mm2 [mean+/-SD], SHR-NF 3.41+/-1.05, SHR-F 2.87+/-0.26; SHR-NF and SHR-F P<0.05 versus WKY rats). The passive stiffness was greater in SHR-F than in the WKY and SHR-NF groups (central segment exponential stiffness constant, Kcs: SHR-F 70+/-25, SHR-NF 44+/-17, WKY 41+/-13 [mean+/-SD]; SHR-F P<0.05 versus SHR-NF and WKY rats). AT did not improve after 10, 20, and 30 minutes of exposure to colchicine (10(-5), 10(-4), and 10(-3) mol/L) in any group. In the SHR-F group, AT and passive stiffness did not change after 30 to 90 minutes of colchicine exposure (10(-4) mol/L). In summary, the data in this study fail to demonstrate improvement of intrinsic muscle function in SHR with heart failure after colchicine. Thus, in the SHR there is no evidence that colchicine-induced cardiac microtubular depolymerization affects the active or passive properties of hypertrophied or failing left ventricular myocardium.

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Several pathologies have been diagnosed in children of hypertensive mothers; however, some studies that evaluated the alterations in their oral health are not conclusive. This study analyzed the salivary gland activity and dental mineralization of offsprings of spontaneously hypertensive rats (SHR). Thirty-day-old SHR males and Wistar rats were studied. The salivary flow was evaluated by injection of pilocarpine, the protein concentration and salivary amylase activity, by the Lowry method and kinetic method at 405 nm, respectively. Enamel and dentin mineralization of the mandibular incisors was quantified with aid of the microhardness meter. The results were analyzed by the ANOVA or Student's t test (p<0.05). It was noticed that the salivary flow rate (0.026 mL/min/100 g ± 0.002) and salivary protein concentration (2.26 mg/mL ± 0.14) of SHR offspring were reduced compared to Wistar normotensive offspring (0.036 mL/min/100 g ± 0.003 and 2.91 mg/mL ± 0.27, respectively), yet there was no alteration in amylase activity (SHR: 242.4 U/mL ± 36.9; Wistar: 163.8 U/mL ± 14.1). Microhardness was lower both in enamel (255.8 KHN ± 2.6) and dentin (59.9 KHN ± 0.8) for the SHR teeth compared to the Wistar teeth (enamel: 328.7 KHN ± 3.3 and dentin: 67.1 KHN ± 1.0). These results suggest that the SHR offspring are more susceptible to development of pathologies impairing oral health, once they presented lesser flow and salivary protein concentration and lower dental mineralization.

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Introduction: The urgent need for studies using standardized protocols to evaluate the real biological effects of PRP has been emphasized by several authors. Objective: The purpose of this study was to standardize a methodology for autologous Platelet-Rich Plasma (PRP) preparation in rats. Material and methods: Twentyfour, 5 to 6-month-old, male rats, weighing 450 to 500 g were used. After general anesthesia, 3.15 ml of blood was collected from each animal, via cannulation of the jugular vein. A standardized technique of double centrifugation was used to prepare PRP. PRP samples and peripheral blood platelets were then manually counted using a Neubauer chamber. Student’s t-test was used to compare the differences between the number of platelets in peripheral blood and PRP samples (p < 0.05). In addition, PRP and peripheral blood smears were stained to see platelets’ morphology. Results: All surgical procedures were well tolerated by the animals and they were healthy during the entire experimental period. PRP samples showed higher significantly platelet concentrations than peripheral blood samples (2,677,583 and 683,680 respectively). Conclusion: Within the limits of this study, it can be concluded that the method used produced autologous PRP with appropriated platelet quantity and quality, in rats.

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Food restriction reduces body weight and influence bone mass and also is correlated with bone mineral density (BMD). Mechanisms have been proposed for the loss of BMD after body weight reduction, including reduced energy intake. Growing 8 wk-old Wistar male rats were randomly divided into Control and Calorie restriction associated with sucrose 30% (CRS). These animals were subjected to intermittent food restriction during 8 weeks and had free access to tap water and sucrose30% in distilled water. The rats were euthanized at the end of week 8, blood collected from abdominal aorta artery, femurs cleaned of adherent soft tissues, scanned using dual energy X-ray absorptiometry, structural and material properties determined by three-point bending testing in the mid-diaphyseal region, bone surface tested in a microhardness tester and microstructure was assessed in a microcomputer tomography. In CRS animals body weight decreased significantly relative to the Control animals. There was a clear option for high-sucrose beverage in CRS animals. No difference was observed in biochemical, densitometric and biomechanical analyzes. Results from micro CT showed only significant difference in connectivity of trabecular bone. It has been suggested that rats submitted to food restriction consumed sugar not because of its inherent palatability, but in order to alter their macronutrient balance and animals need to meet energy demands in high-sucrose.

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

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Objective: The aim of this study was assess the role of chronic stress on the metabolic and nutritional profile of rats exposed to a high-fat diet. Materials and methods: Thirty-day-old male Wistar rats (70-100 g) were distributed into four groups: normal-diet (NC), chronic stress (St), high-fat diet (HD), and chronic stress/high-fat diet (HD/St). Stress consisted at immobilization during 15 weeks, 5 times per week, 1h per day; and exposure to the high-fat diet lasted 15 weeks. Nutritional and metabolic parameters were assessed. The level of significance was 5%. Results: The HD group had final body weight, total fat, as well as insulin and leptin increased, and they were insulin resistant. The St and HD/St had arterial hypertension and increased levels of corticosterone. Stress blocked the effects of the high-fat diet. Conclusion: Chronic stress prevented the appearance of obesity. Our results help to clarify the mechanisms involved in metabolic and nutritional dysfunction, and contribute to clinical cases linked to stress and high-fat diet.