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OBJECTIVE: Feeding intolerance, manifesting as increased gastric residual, is a common finding in preterm neonates. Little is known about the regulation of gastric emptying early in life and the extent to which this plays a role in the preterm infants' feeding tolerance. The goal of this study was to evaluate clinically stable 28- to 32-week gestation neonates during the first 4 weeks of life and noninvasively determine their gastric emptying rate. STUDY DESIGN: Ultrasound measurements of gastric milk content volume were obtained from 25 neonates immediately after, 30 and/or 60 minutes following routine gavage feeds. The content emptying rate was calculated from the gastric volume data. RESULTS: Gastric emptying rate was not postnatal age-dependent, was significantly higher at 30 minutes, whenever compared with 60-minute postfeed and directly proportional to the feed volume. At any postnatal age, the gastric emptying rate was at least 6-fold greater, when comparing the lowest and highest average stomach content volumes. CONCLUSIONS: The gastric emptying rate of preterm infants is content volume-dependent and unrelated to the postnatal age. Given the present findings, further investigation on the gastric residual of preterm infants receiving larger than currently administered feed volumes at the initiation of enteral nutrition, is warranted.

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OBJETIVOS: Embora reconhecida há décadas, ainda pouco se sabe a respeito da etiologia, fisiopatologia e prevenção da hipertensão pulmonar persistente neonatal (HPPN), e seu tratamento continua a ser um grande desafio para os neonatologistas. Nesta revisão, vamos abordar as características clínicas e os mecanismos fisiopatológicos da síndrome, assim como seu tratamento geral e específico. FONTES DE DADOS: Fizemos uma revisão nas bases de dados PubMed, Cochrane Library e MRei Consult , procurando por artigos relacionados à síndrome e publicados entre 1995 e 2011. SÍNTESE DE DADOS: São discutidos os fatores de risco e os mecanismos fisiopatológicos da síndrome. O quadro clínico depende dos diferentes fatores envolvidos, que provavelmente estão relacionados com a etiologia e o mecanismo fisiopatológico. Além das medidas utilizadas para permitir a queda da resistência vascular pulmonar após o nascimento, alguns casos necessitam de vasodilatadores pulmonares. Embora o óxido nítrico tenha se provado efetivo, recentemente, outros vasodilatadores têm sido usados, mas ainda faltam evidências clínicas para comprovar seus benefícios no tratamento da HPPN. CONCLUSÕES: Apesar dos recentes avanços tecnológicos e dos novos conhecimentos fisiopatológicos, a mortalidade associada à HPPN ainda é de 10%. São necessárias mais pesquisas clínicas e resultados experimentais baseados em evidências para prevenir, tratar e reduzir a morbimortalidade associada a esta síndrome neonatal.

OBJECTIVES: Although recognized for decades, little is known about the etiology, physiopathology, and prevention of persistent pulmonary hypertension of the newborn (PPHN). and its treatment remains a major challenge for neonatologists. In this review, the clinical features and physiopathology of the syndrome will be addressed, as well as its general and specific treatments. DATA SOURCE: A review was carried out in PubMed, Cochrane Library, and MRei consult databases, searching for articles related to the syndrome and published between 1995 and 2011. DATA SYNTHESIS: Risk factors and the physiopathological mechanisms of the syndrome are discussed. The clinical picture depends on the different factors involved, which are probably related to the etiology and physiopathological mechanisms. In addition to the measures used to allow the decrease in pulmonary vascular resistance after birth, some cases will require pulmonary vasodilators. Although nitric oxide has proved effective, other vasodilators have been recently used, but clinical evidence is still lacking to demonstrate their benefits in the treatment of PPHN. CONCLUSIONS: Despite recent technological advances and new physiopathological knowledge, mortality associated with PPHN remains at 10%. More clinical research and evidence-based experimental results are needed to prevent, treat, and reduce the morbidity/mortality associated with this neonatal syndrome.

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OBJECTIVES: Although recognized for decades, little is known about the etiology, physiopathology, and prevention of persistent pulmonary hypertension of the newborn (PPHN), and its treatment remains a major challenge for neonatologists. In this review, the clinical features and physiopathology of the syndrome will be addressed, as well as its general and specific treatments. DATA SOURCE: A review was carried out in PubMed, Cochrane Library, and MRei consult databases, searching for articles related to the syndrome and published between 1995 and 2011. DATA SYNTHESIS: Risk factors and the physiopathological mechanisms of the syndrome are discussed. The clinical presentation depends on the different factors involved. These are related to the etiology and physiopathology of the different forms of the disease. In addition to the measures used to allow for the decrease in pulmonary vascular resistance after birth, in some instances pulmonary vasodilators will be required. Although inhaled nitric oxide has proved effective, other vasodilators have been recently used, but clinical evidence is still lacking to demonstrate their benefits in the treatment of PPHN. CONCLUSIONS: Despite recent technological advances and new physiopathological knowledge of this disease, mortality associated with PPHN remains at 10%. More clinical research and evidence-based experimental results are needed to prevent, treat, and reduce the morbidity/mortality associated with this neonatal syndrome.

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Breast milk reduces the incidence of necrotizing enterocolitis (NEC). BH4 is a cofactor for endothelial NOS (eNOS). Reduced BH4 levels, or its oxidation to dihydrobiopterin (BH2), uncouple eNOS resulting in formation of reactive oxygen species (ROS) that have been implicated in the pathogenesis of NEC. We evaluated colostrum and mature breast milk, as well as infant formula, BH4 and BH2 content. In addition, we tested the BH4 effect on the newborn rat mesenteric arterial vascular tone. BH4 and BH2 content increased 3-fold in mature breast milk, when compared with colostrum (p < 0.01), without a change in their ratio. Infant formula had a negligible BH4 content and lower biopterins ratio, when compared with breast milk. eNOS is the predominant synthase isoform in newborn rat mesenteric arteries. In the presence of BH4, mesenteric arteries contracted less to thromboxane A2 analog U46619 (p < 0.01) and this effect was abolished following eNOS inhibition. BH4 (10⁻6 M) vasorelaxed the newborn rat mesenteric arteries. We conclude that when compared with infant formula, breast milk has a high BH4 content that increases as breastfeeding continues. Given its mesenteric arterial vasorelaxing effect, BH4 may play an important role in the reduced NEC incidence among breast fed infants.

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OBJECTIVES: peritoneal fluid accumulation is a common finding in many children with abdominal disorders and its generation secondary to increased vascular permeability. The contribution of the arterial versus venous circulation to edema formation and peritoneal fluid accumulation is poorly understood. Studies conducted in vivo more than two decades ago suggested that the postcapillary venules were more important than the arterial vessels in the process of edema formation. The purpose of the present study as to evaluate the effect of changes in intravascular pressure and the inflammatory mediator bradykinin on rat mesenteric arterial and venous vascular permeability. METHOD: mesenteric arteries (MA) and veins (MV) were mounted on glass cannulas, intravascularly filled with fluorescent dextran and incrementally pressurized above their in vivo physiological values. Vascular permeability to dextran was determined at 100, 200 and 300 percent of physiological pressures. RESULT: vascular permeability was present at all measurements for both vessels and its magnitude directly proportional to the intravascular pressure. Bradykinin (10-5 M) significantly increased permeability in the MV but not in the MA. CONCLUSION: the abdominal fluid accumulation related to bowel inflammatory disease is more likely to be secondary to venous, as opposed to arterial vascular leakage.(AU)

OBJETIVO: o acúmulo de líquido peritoneal é um achado comum em muitas crianças com distúrbios abdominais e sua geração é secundária ao aumento da permeabilidade vascular. A contribuição da circulação arterial versus venosa para a formação de edema e acúmulo de líquido peritoneal é mal compreendida. Estudos realizados in vivo mais de duas décadas atrás, sugeriram que a vênulas são mais importantes que os vasos arteriais no processo de formação de edema. O objetivo deste trabalho é analisar os efeitos das mudanças na pressão intravascular e a inflamação mediada pela bradicinina na permeabilidade venosa e vascular mesentérica de ratos. MÉTODO: artérias mesentéricas (MA) e veias (MV) foram montadas em cânulas de vidro, por via intravenosa preenchida com dextran fluorescentes e incremental pressurizado acima de seus valores fisiológicos in vivo. Permeabilidade vascular para dextrana foi determinada a 100, 200 e 300 por cento de pressões fisiológicas. RESULTADOS: a permeabilidade vascular estava presente em todas as medidas para ambos os vasos e sua magnitude diretamente proporcional à pressão intravascular. A bradicinina (10-5 M) aumentou significativamente a permeabilidade da MV, mas não no MA. CONCLUSÃO: o acúmulo de líquido abdominal relacionado à doença inflamatória intestinal é mais provável de ser secundária a venosa, em oposição à fuga vascular arterial.(AU)

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OBJETIVO: o acúmulo de líquido peritoneal é um achado comum em muitas crianças com distúrbios abdominais e sua geração é secundária ao aumento da permeabilidade vascular. A contribuição da circulação arterial versus venosa para a formação de edema e acúmulo de líquido peritoneal é mal compreendida. Estudos realizados in vivo mais de duas décadas atrás, sugeriram que a vênulas são mais importantes que os vasos arteriais no processo de formação de edema. O objetivo deste trabalho é analisar os efeitos das mudanças na pressão intravascular e a inflamação mediada pela bradicinina na permeabilidade venosa e vascular mesentérica de ratos. MÉTODO: artérias mesentéricas (MA) e veias (MV) foram montadas em cânulas de vidro, por via intravenosa preenchida com dextran fluorescentes e incremental pressurizado acima de seus valores fisiológicos in vivo. Permeabilidade vascular para dextrana foi determinada a 100, 200 e 300 por cento de pressões fisiológicas. RESULTADOS: a permeabilidade vascular estava presente em todas as medidas para ambos os vasos e sua magnitude diretamente proporcional à pressão intravascular. A bradicinina (10-5 M) aumentou significativamente a permeabilidade da MV, mas não no MA. CONCLUSÃO: o acúmulo de líquido abdominal relacionado à doença inflamatória intestinal é mais provável de ser secundária a venosa, em oposição à fuga vascular arterial

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OBJECTIVES: Sildenafil, a phosphodiesterase-5 inhibitor, significantly improves oxygenation when used in animal models and patients with pulmonary hypertension. Tadalafil is a new and clinically available phosphodiesterase-5 inhibitor that, aside from causing pulmonary vasodilation, has been shown to increase cardiac output in pulmonary hypertensive adults. Its hemodynamic effects on the newborn, however, have not been tested. The objective was to evaluate the effect of tadalafil on central hemodynamics and arterial oxygenation in a piglet model of acute pulmonary hypertension. DESIGN: Laboratory experiment. SETTING: University laboratory. SUBJECTS: Seven anesthetized and mechanically ventilated newborn piglets. INTERVENTIONS: Pulmonary hypertension was induced and maintained in seven anesthetized and mechanically ventilated newborn piglets following acute exposure to 11% oxygen. The experimental animals received orla tadalafil (1 mg/kg), whereas the control animals were given an equal volume of normal saline. Systemic and pulmonary hemodynamic variables were measured, and the cardiac output and ejection fraction were obtained from two-dimensional echocardiogram and Doppler measurements in all animals. Serial arterial blood gases were also obtained, and the alveolar-arterial oxygen gradient was calculated. MEASUREMENTS AND MAIN RESULTS: In contrast with the control animals, in which no significant changes were noted, in the experimental animals pulmonary arterial pressure decreased on average by 54% and cardiac output increased by 88% following tadalafil administration (p < .05). Tadalafil increased the PaO2 by 48% +/- 21% (p < .01), likely as a result of a 74% +/- 13% reduction in the alveolar-arterial oxygen gradient (p < .01). CONCLUSIONS: In a newborn animal model of acute pulmonary hypertension, oral tadalafil administration reduces pulmonary vascular resistance and increases arterial oxygenation by increasing cardiac output and reducing the lung shunt fraction. This previously untested compound deserves additional investigation in laboratory models of persistent pulmonary hypertension of the newborn.

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