Effects of antioxidant MnTBAP on angiogenesis in newborn mice with hyperoxic lung injury.

BACKGROUND: Oxygen toxicity mediated by reactive oxygen species (ROS) plays an essential role in the development of bronchopulmonary dysplasia in premature infants. By reducing oxidative stress, antioxidants protect the immature lung. We studied the effects of MnTBAP, a catalytic antioxidant on angiogenesis and alveolar growth following neonatal hyperoxia. METHODS: Newborn mouse litters randomized to room air (RA) or >95% O2 for 72 hours from day 4 (D4) to D7 to receive either MnTBAP (10 mg/kg/d) or saline intraperitoneally (every 24 h for three doses). Lungs harvested for angiogenic gene expression, protein expression, and histopathology post-hyperoxia exposure. Radial alveolar count (RAC), mean linear intercept (MLI) and vessel density assessed by histopathology. RESULTS: Angiogenic gene expression was significantly lower in the hyperoxia group compared to the RA group. The protein expression for VEGF and its receptor, VEGFR1, was significantly lower following treatment with MnTBAP compared to hyperoxia alone. Expression of VEGFR2, Angiopoietin-1 and TIE2, were substantially higher in the RA groups compared to hyperoxia groups with or without MnTBAP. Hyperoxia groups demonstrated alveolar simplification. MnTBAP reduced vessel density and failed to improve alveolar growth following hyperoxia. CONCLUSIONS: MnTBAP, a catalytic antioxidant, does not offer protection from hyperoxia-induced alveolar impairment. The lack of angiogenic upregulation by MnTBAP may contribute to alveolar simplification in newborn mice.

Stridor in infants with hypoxic-ischemic encephalopathy and whole body hypothermia: A case series.

BACKGROUND: Stridor is one of the rare side effects of neonatal hypothermia treatment for hypoxic-ischemic encephalopathy. We aimed to describe the clinical characteristics of the infants who underwent whole-body hypothermia and developed stridor. METHODS: We reviewed the medical records of 171 infants with moderate or severe hypoxic-ischemic encephalopathy who underwent hypothermia therapy. Demographics, as well as clinical characteristics, were documented. RESULTS: A total of 18 infants developed transient stridor out of 171 infants who underwent whole-body hypothermia (10.5%). The stridor was transient and resolved in all infants. All infants with stridor received treatment with one or more of the following: racemic epinephrine, dexamethasone, positive pressure ventilation and/or heliox. Two infants required otorhinolaryngologist (ENT) evaluation due to persistent and severe symptoms, of whom one was found to have left vocal cord paresis that improved with time. CONCLUSION: Stridor is a transient complication associated with hypoxic-ischemic encephalopathy and whole-body hypothermia in neonates. The exact mechanism is unclear and most likely multifactorial. ENT evaluation is recommended in the presence of prolonged symptoms or significant respiratory distress.

Early onset necrotizing enterocolitis (NEC) in premature twins.

Twin infants born at 34 week gestation had frank blood in stools on day three of life on mixed feeds of formula and maternal breast milk. Sepsis work up was negative in these relatively well appearing infants with pneumatosis in the colon on abdominal x-ray. Blood in stools recurred on reintroduction of breast milk in Twin A. Both infants recovered from episodes of bloody stools on amino-acid based formula and were thriving at discharge. Early necrotizing enterocolitis in both twins is rare and has not been reported. Cow's milk protein sensitivity, possibly from in-utero sensitization, could explain non-infectious colitis in these twins, precipitated by formula or breast milk after birth.