983 resultados para Mortalidade Neonatal
Resumo:
This study aimed to investigate the in vivo and in vitro reactivity of airway smooth muscle in rats depleted of sensory neuropeptides by treatment with capsaicin at neonatal stage. Wistar rats were neonatally injected with either capsaicin (50 mg/kg, s.c., 2nd day of life) or its vehicle (10% ethanol and 10% Tween 80, in 0.9% w/v NaCl solution) and used at adult ages (60-70 days later). Analysis of the lungs showed a higher number of infiltrating neutrophils, eosinophils and mononuclear cells into the peribronchiolar regions of capsaicin-pretreated rats compared to vehicle group. This was associated with a higher contraction index of bronchiolar wall in the capsaicin group. The in vitro tracheal reactivity in response to methacholine (full muscarinic agonist) and pilocarpine (partial muscarinic agonist) was also significantly higher in capsaicin-pretreated rats compared to vehicle group. In conclusion, the neuropeptide depletion by capsaicin neonatal treatment lead to marked contraction of the rat airways at adult age, suggesting a protective role for C fibers in the lungs. (C) 2003 Elsevier B.V. Ireland Ltd. All rights reserved.
Resumo:
We studied the development of the insulin secretion mechanism in the pancreas of fetal (19- and 21-day-old), neonatal (3-day-old), and adult (90-day-old) rats in response to stimulation with 8.3 or 16.7 mM glucose, 30 mM K+, 5 mM theophylline (Theo) and 200 µM carbamylcholine (Cch). No effect of glucose or high K+ was observed on the pancreas from 19-day-old fetuses, whereas Theo and Cch significantly increased insulin secretion at this age (82 and 127% above basal levels, respectively). High K+ also failed to alter the insulin secretion in the pancreas from 21-day-old fetuses, whereas 8.3 mM and 16.7 mM glucose significantly stimulated insulin release by 41 and 54% above basal levels, respectively. Similar results were obtained with Theo and Cch. A more marked effect of glucose on insulin secretion was observed in the pancreas of 3-day-old rats, reaching 84 and 179% above basal levels with 8.3 mM and 16.7 mM glucose, respectively. At this age, both Theo and Cch increased insulin secretion to close to two-times basal levels. In islets from adult rats, 8.3 mM and 16.7 mM glucose, Theo, and Cch increased the insulin release by 104, 193, 318 and 396% above basal levels, respectively. These data indicate that pancreatic B-cells from 19-day-old fetuses were already sensitive to stimuli that use either cAMP or IP3 and DAG as second messengers, but insensitive to stimuli such as glucose and high K+ that induce membrane depolarization. The greater effect of glucose on insulin secretion during the neonatal period indicates that this period is crucial for the maturation of the glucose-sensing mechanism in B-cells.
Resumo:
Background: Animal models appear well-suited for studies into the role of exercise in the prevention of non-insulin-dependent diabetes mellitus (NIDDM). The aim of the present study was to analyze glucose homeostasis and blood lactate during an exercise swimming test in rats treated with alloxan during the neonatal period and/or fed a high calorie diet from weaning onwards.Methods: Rats were injected with alloxan (200 mg/kg, i.p.) or vehicle (citrate buffer) at 6 days of age. After weaning, rats were divided into four groups and fed either a balanced diet or a high-caloric diet as follows: C, control group (vehicle + normal diet); A, alloxan-treated rats fed the normal diet; H, vehicle-treated rats fed the high-caloric diet; and HA, alloxan-treated rats fed the high-caloric diet.Results: Fasting serum glucose levels were higher in groups A and AH compared with the control group. The Homeostatic Model Assessment index varied in the groups as follows: H > A > HA = C. There were no differences in free fatty acids or blood lactate concentrations during the swim test.Conclusions: Alloxan-treated rats fed a normal or high-caloric diet have the potential to be used in studies analyzing the role physical exercise plays in the prevention of NIDDM.
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Resumo:
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)