INTRODUCTIONElastic and collagen fiber deposition increases throughout normal lung development, and this fiber network significantly changes when development of the lung is disturbed. In preterm rats and lambs, prolonged hyperoxic exposure is associated with impaired alveolization and causes significant changes in the deposition and structure of elastic fibers.OBJECTIVESTo evaluate the effects of hyperoxic exposure on elastic and collagen fiber deposition in the lung interstitial matrix and in alveolarization in preterm rabbits.METHODSAfter c-section, 28-day preterm New-Zealand-White rabbits were randomized into 2 study groups, according to the oxygen exposure, namely: Room air (oxygen = 21%) or Oxygen (oxygen ≥ 95%). The animals were killed on day 11 and their lungs were analyzed for the alveolar size (Lm), the internal surface area (ISA), the alveoli number, and the density and distribution of collagen and elastic fibers.RESULTSAn increase in the Lm and a decrease in the alveoli number were observed among rabbits that were exposed to hyperoxia with no differences regarding the ISA. No difference in the density of elastic fibers was observed after oxygen exposure, however there were fewer collagen fibers and an evident disorganization of fiber deposition.DISCUSSIONThis model reproduces anatomo-pathological injuries representing the arrest of normal alveolar development and lung architecture disorganization by just a prolonged exposition to oxygen.CONCLUSIONSIn the preterm rabbit, prolonged oxygen exposure impaired alveolization and also lowered the proportion of collagen fibers, with an evident fiber network disorganization.

Objectives: To analyze the effects of nutritional restriction and hyperoxia on lung weight and pulmonary morphometry in premature rabbits during the first 11 days of life.Methods: New Zealand White rabbits were delivered by C-section at 28 days gestational age and randomized into four groups: control diet and room air, control diet and hyperoxia (> 95% O 2 ), nutritional restriction and room air and nutritional restriction and hyperoxia (> 95% O 2 ). Nutritional restriction was achieved by reducing all nutrients by 30% in comparison with the control diet. Lung tissue slides were stained with hematoxylin-eosin, modified resorcin-orcein and picrosirius, before morphometric analysis was performed.Results: From the fourth day onwards, less weight was gained by the nutritional restriction and hyperoxia group (p < 0.001), and from the sixth day on, by the nutritional restriction and room air group (p < 0.001), in comparison with their respective control groups. Nutritional restriction decreased alveoli number (p < 0.001) and collagen deposition (p < 0.001). Hyperoxia was responsible for reductions in number of alveoli (p < 0.001) and collagen deposition (p < 0.001), in addition to higher mean linear intercept values (p < 0.05) and thickening of alveolar septa (p < 0.001). When nutritional restriction was associated with hyperoxia, the reductions in number of alveoli (p < 0.001) and of collagen deposition (p < 0.001) intensified.Conclusions: Nutritional restriction intensified the changes of pulmonary architecture findings caused by hyperoxia, in particular through alterations to alveolarization and collagen deposition. ResumoObjetivos: Este modelo experimental foi desenvolvido para analisar os efeitos da restrição nutricional e da hiperoxia, durante 11 dias, sobre o peso e a morfometria pulmonares, em coelhos prematuros.Métodos: Após cesárea, coelhos New Zealand White com idade gestacional de 28 dias foram randomizados nos seguintes grupos: dieta controle e ar ambiente, dieta controle e hiperoxia (> 95% O 2 ), restrição nutricional e ar ambiente e restrição nutricional e hiperoxia (> 95% O 2 ). A restrição nutricional foi obtida com uma redução em 30% de todos os nutrientes da dieta controle. As lâminas de pulmão foram coradas com hematoxilina-eosina, resorcina-orceína modificada e picrosírius, sendo posteriormente realizada a análise morfométrica.Resultados: Observou-se um menor ganho de peso no grupo restrição nutricional e hiperoxia (p < 0,001) a partir do quarto dia e, no grupo restrição nutricional e ar ambiente (p < 0,001), a partir do sexto dia de vida, em relação aos respectivos grupos controles. A restrição nutricional reduziu o número de alvéolos (p < 0,001) e o depósito de colágeno (p < 0,001). A hiperoxia produziu uma redução do número de alvéolos (p < 0,001) e do depósito de colágeno (p < 0,001), além de maiores intercepto linear médio (p < 0,05) e espessamento de septos inter-alveolares (p < 0,001). A restrição nutricional associada à hiperoxia intensificou a redução do número de alvéolos (p < 0...

Several factors are associated with bronchopulmonary dysplasia. Among them, hyperoxia and lung immaturity are considered to be fundamental; however, the effect of malnutrition is unknown. Our objective was to evaluate the effects of 7 days of postnatal malnutrition and hyperoxia on lung weight, volume, water content, and pulmonary morphometry of premature rabbits. After csection, 28-day-old New Zealand white rabbits were randomized into four groups: control diet and room air (CA, N = 17), control diet and ≥95% O 2 (CH, N = 17), malnutrition and room air (MA, N = 18), and malnutrition and ≥95% O 2 (MH, N = 18). Malnutrition was defined as a 30% reduction of all the nutrients provided in the control diet. Treatments were maintained for 7 days, after which histological and morphometric analyses were conducted. Lung slices were stained with hematoxylin-eosin, modified orcein-resorcin or picrosirius. The results of morphometric analysis indicated that postnatal malnutrition decreased lung weight (CA: 0.83 ± 0.19; CH: 0.96 ± 0.28; MA: 0.65 ± 0.17; MH: 0.79 ± 0.22 g) and water content, as well as the number of alveoli (CA: 12.43 ± 3.07; CH: 8.85 ± 1.46; MA: 7.33 ± 0.88; MH: 6.36 ± 1.53 x 10 -3 /mm) and elastic and collagen fibers. Hyperoxia reduced the number of alveoli and increased septal thickening and the mean linear intercept. The reduction of alveolar number, collagen and elastic fibers was intensified when malnutrition and hyperoxia were associated. These data suggest that dietary restriction enhances the magnitude of hyperoxia-induced alveolar growth arrest and lung parenchymal remodeling. It is interesting to consider the important influence of postnatal nutrition upon lung development and bronchopulmonary dysplasia.

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Schinzel-Giedion syndrome is a rare autosomal recessive disorder characterized by coarse facies, midface retraction, hypertrichosis, multiple skeletal anomalies, and cardiac and renal malformations. Craniofacial abnormalities of this syndrome sometimes resemble a storage or metabolic disease. The pathogenesis of the disease remains unknown. The objective of this report was to emphasize the importance of congenital bilateral hydronephrosis for the diagnosis of Schinzel-Giedion syndrome. We describe the first Brazilian case of a newborn with typical facies, generalized hypertrichosis, cardiac and skeletal anomalies, and bilateral hydronephrosis detected during pregnancy and confirmed later by abdominal ultrasonography. Chromosomal constitution was normal. Of the 35 cases already reported in the literature, 31 presented hydronephrosis, which is considered an important clue in diagnosis. If Schinzel-Giedion syndrome were indexed as a cause of congenital hydronephrosis, its identification would be greatly facilitated, since the majority of the other findings in Schinzel-Giedion syndrome are nonspecific and common to many genetic syndromes.

RESULTS: The incidence of bronchopulmonary dysplasia was 6.5% (Group I) and 30% (Group II), P = .07. A decrease in growth was detected in Group I compared with Group II (change in weight: Group I -47 g/week, Group II -85.5 g/week, P = .06; change in head circumference: Group I -0.75 cm/week, Group II -1 cm/week, P = .05).CONCLUSION: Use of corticosteroids in very low birth weight infants dependent on mechanical ventilation during the first 10 to 14 days of life did not affect the respiratory evolution and occurrence of bronchopulmonary dysplasia, but the velocity of growth was reduced.KEYWORDS: Corticosteroids. Very low birth weight newborn. Bronchopulmonary dysplasia.

SUMMARY: Ventilator-dependent premature infants are often treated with dexamethasone. Several trials showed that steroids while improve pulmonary compliance and facilitate extubation, some treated infants may have adverse effects, such as alterations of growth curves. We conducted this retrospective study to evaluate the effects of steroids on mechanical ventilation, oxygen therapy, hospital length stay and mortality, in ventilator-dependent infants with bronchopulmonary dysplasia (BPD) (defined as the need of oxygen supplementation at 28 days of life). Twenty-six newborns with BPD were evaluated during 9 -42 days postpartum (mean = 31 days) and were divided into two groups: Group I -14 newborns that did not receive dexamethasone, and Group II -12 newborns that received dexamethasone at 14 -21 days of life. Dexamethasone was given at a dose of 0.25 mg per kilogram of body weight twice daily intravenously for 3 days, after which the dose was tapered.Results -There were no statistically significant differences in the mean length of mechanical ventilation (Group I -37 days, Group II -35 days); oxygen supplementation (Group I -16 days, Group II -29 days); hospital stay (Group I -72 days, Group II -113 days); mortality (Group I -35.7%, Group II -41.6%).At birth, Group II was lighter (BW: Group I -1154 grams ± 302, Group II -791 grams ± 165; p < 0.05) and smaller (height: Group I -37.22 cm ± 3.3, Group II -33.5 ± 2.4; p< 0.05) than Group I.At 40 weeks, there were no statistically significant differences between groups in relation to anthropometric measurements. Conclusions -The use of corticosteroids in bronchopulmonary dysplasic infants may influence the somatic growth during its use. However, after its suspension, a recovery seems to occur, suggesting that its influence could be transitory. DESCRIPTORS: Dexamethasone therapy. Bronchopulmonary dysplasia.

ResumoObjetivo: Avaliar um esquema de abordagem ao nascimento de recém-nascidos cujas mães tivessem ruptura de membranas (RPM) por 24 horas ou mais antes do parto, com base em parâmetros, clínicos e laboratoriais selecionados, de infecção neonatal.Métodos: Estudo prospectivo, incluindo recém-nascidos admitidos no Berçário Anexo à Maternidade (HC -FMUSP) no período de maio de 1993 a dezembro de 1994, cujas mães tivessem RPM > 24 horas. Em todos os recém-nascidos realizou-se hemograma (cordão umbilical e 24 horas) e hemocultura (cordão umbilical). Receberam antibioticoterapia os recém-nascidos com sinais clíni-cos de corioamnionite, IG < 34 semanas e/ou IG > 34 semanas e < 37 semanas, na presença de fatores de risco para infecção. Os recém-nascidos incluídos foram distribuídos em 4 subgrupos: GI (RPM < 48 horas), GII (RPM > 48 horas e < 7 dias), GIII (RPM > 7 dias e < 14 dias), GIV (RPM > 14 dias).Resultados: A incidência de infecção nos RN foi de 38,1%, tendo sido maior, de forma estatisticamente significante (p < 0,05) nos recém-nascidos com IG < 34 semanas. Não houve diferença estatisticamente significante entre os subgrupos. Dentre os fatores de risco analisados, a IG < 34 semanas foi o indicador mais importante de risco infeccioso.Conclusões: Os autores recomendam o uso de antibioticoterapia profilática na presença de RPM em recém-nascidos com IG < 34 semanas, a fim de reduzir o risco de infecção neonatal. J. pediatr. (Rio J.). 1997; 73(5):311-316: ruptura prolongada de membrana, rotura prolongada de membrana, amniorrexis, infecção neonatal, infecção amniótica. AbstractObjective: To evaluate a schedule of assesment at birth of newborn from mothers with prolonged rupture of membranes (PROM > 24 hours), based on selected clinical and laboratorial parameters of infection.Methods: Prospective study, including newborns admitted to