Risk Factors of Massive Pulmonary Hemorrhage in Newborn Infants / 대한주산의학회잡지

OBJECTIVES: Massive pulmonary hemorrhage (MPH) is a lethal disease, that large amount of blood is spouted from lung with clinical exacerbation, leading to death in newborn infants. Many of its causes were proved but debated. The purpose of this study is to determine the risk factors of Massive pulmonary hemorrhage of the newborn infants. We defined Mild pulmonary hemorrhage (mPH) as small amount of bleeding from lung with no changes in patient's clinical status. METHODS: Risk factors of MPH were estimated by retrospective multivariable analysis among newborn infants with pulmonary hemorrhage in neonatal intensive care unit of Catholic University Hospital of Daegu from January 2001 to December 2007. RESULTS: Pulmonary hemorrhage was developed in 73 neonates (6.3% of total infants admitted to NICU during the study period) and MPH occurred in 25 neonates (34.2%). Gestational age and Birth weights were lower in neonate with MPH than those with mPH. Thrombocytopenia and hypotension were statistically higher in those with MPH than mPH. There were no different significances between MPH and mPH in mean Bomsel grades of respiratory distress syndrome (RDS), Asphyxia, sepsis, disseminated intravascular coagulopathy (DIC), persistent ductus arteriosus (PDA), and intraventricular hemorrhage (IVH). CONCLUSION: The risk factors for massive pulmonary hemorrhage in newborn infants might be thrombocytopenia, and hypotension.

Neuroprotective Effect of Dizocilpine (MK-801) via Anti-apoptosis on Hypoxic-ischemic Brain Injury in Neonatal Rats

PURPOSE: Current studies have demonstrated the neuroprotective effects of dizocilpine (MK-801) in many animal models of brain injury, including hypoxic-ischemic (HI) encephlopathy, trauma and excitotoxicity, but limited data are available for those during the neonatal periods. Here we investigated whether dizocilpine can protect the developing rat brain from HI injury via anti-apoptosis. METHODS: In an in vitro model, embryonic cortical neuronal cell culture of Sprague-Dawley (SD) rats at 18-day gestation was done. The cultured cells were divided into three groups: normoxia (N), hypoxia (H), and hypoxia treated with dizocilpine (HD). The N group was prepared in 5% CO2 incubators and the other groups were placed in 1% O2 incubators (94% N2, 5% CO2) for 16 hours. In an in vivo model, left carotid artery ligation was done in 7-day-old SD rat pups. The animals were divided into six groups; hypoxia (N), hypoxia (H), hypoxia with sham-operation (HS), hypoxia with operation (HO), HO treated with vehicle (HV), and HO treated with dizocilpine (HD). Hypoxia was made by exposure to a 2 hour period of hypoxic incubator (92% N2, 8% O2). RESULTS: In the in vitvo and in vivo models, the expressions of Bcl-2 in the hypoxia groups were reduced compared to the normoxia group. whereas those in the dizocilpine-treated group were increased compared to the hypoxia group. However. the expressions of Bax and caspase-3 and the ratio of Bax/Bcl-2 were revealed reversely. CONCLUSION: Dizocilpine has neuroprotective property over perinatal HI brain injury via anti-apoptosis.

Neuroprotective Effect of Dizocilpine (MK-801) via Anti-apoptosis on Hypoxic-ischemic Brain Injury in Neonatal Rats

PURPOSE: Current studies have demonstrated the neuroprotective effects of dizocilpine (MK-801) in many animal models of brain injury, including hypoxic-ischemic (HI) encephlopathy, trauma and excitotoxicity, but limited data are available for those during the neonatal periods. Here we investigated whether dizocilpine can protect the developing rat brain from HI injury via anti-apoptosis. METHODS: In an in vitro model, embryonic cortical neuronal cell culture of Sprague-Dawley (SD) rats at 18-day gestation was done. The cultured cells were divided into three groups: normoxia (N), hypoxia (H), and hypoxia treated with dizocilpine (HD). The N group was prepared in 5% CO2 incubators and the other groups were placed in 1% O2 incubators (94% N2, 5% CO2) for 16 hours. In an in vivo model, left carotid artery ligation was done in 7-day-old SD rat pups. The animals were divided into six groups; hypoxia (N), hypoxia (H), hypoxia with sham-operation (HS), hypoxia with operation (HO), HO treated with vehicle (HV), and HO treated with dizocilpine (HD). Hypoxia was made by exposure to a 2 hour period of hypoxic incubator (92% N2, 8% O2). RESULTS: In the in vitvo and in vivo models, the expressions of Bcl-2 in the hypoxia groups were reduced compared to the normoxia group. whereas those in the dizocilpine-treated group were increased compared to the hypoxia group. However. the expressions of Bax and caspase-3 and the ratio of Bax/Bcl-2 were revealed reversely. CONCLUSION: Dizocilpine has neuroprotective property over perinatal HI brain injury via anti-apoptosis.

Neuroprotective effects of resveratrol via anti-apoptosis on hypoxic-ischemic brain injury in neonatal rats / 소아과

PURPOSE: Resveratrol, extracted from red wine and grapes, has an anti-cancer effect, an antiinflammatory effect, and an antioxidative effect mainly in heart disease and also has neuroprotective effects in the adult animal model. No studies for neuroprotective effects during the neonatal periods have been reported. Therefore, we studied the neuroprotective effect of resveratrol on hypoxic-ischemic brain damage in neonatal rats via anti-apoptosis. METHODS: Embryonic cortical neuronal cell culture of rat brain was performed using pregnant Sprague-Dawley (SD) rats at 18 days of gestation (E1 8) for the in vitro approach. We injured the cells with hypoxia and administered resveratrol (1, 10, and 30 microg/mL) to the cells at 30 minutes before hypoxic insults. In addition, unilateral carotid artery ligation with hypoxia was induced in 7 -day-old neonatal rats for the in vivo approach. We injected resveratrol (30 mg/kg) intraperitoneally into animal models. Real-time PCR and Western blotting were performed to identify the neuroprotective effects of resveratrol through anti-apoptosis. RESULTS: In the in vitro approach of hypoxia, the expression of Bax, caspase-3, and the ratio of Bax/Bcl-2, indicators of the level of apoptosis, were significantly increased in the hypoxia group compared to the normoxia group. In the case of the resveratrol-treated group, expression was significantly decreased compared to the hypoxia group. And the results in the in vivo approach were the same as in the in vitro approach. CONCLUSION: The present study demonstrates that resveratrol plays neuroprotective role in hypoxic-ischemic brain damage during neonatal periods through the mechanism of anti-apoptosis.

The expression patterns of nitric oxide synthases (NOS) by resveratrol in hypoxic-ischemic brain injury in neonatal rat model / 대한주산의학회잡지

OBJECTIVE: Resveratrol, a polyphenolic phytoalexin, is extracted abundantly from the red wine and grapes and biosynthesized as a defense agent to infection, ultraviolet and ozon etc. Recently, The cancer-preventive, anti-inflammatory and anti-oxidative effects of resveratrol have been reported. The aim of this study was to investigate the effect of resveratrol on the expression of nitric oxide synthases in hypoxic-ischemic brain injury in the neonatal rat model. METHODS: Embryonic cortical neuronal cell culture of rat brain was performed with pregnant Sprague-Dawley (SD) rats at 18 days of gestation (E18) for in vitro approaches. In addition, unilateral carotid artery ligation was induced in seven-days old neonatal rats for in vivo approaches. The real-time PCR using iNOS, eNOS and nNOS primer, and the western blotting using the same antibodies were done to identify the effects of resveratrol. RESULTS: The expression of iNOS, eNOS and nNOS in both cell culture and animal model of neonatal HI brain injury revealed that, as indicated by western blotting and real-time PCR, the expression of iNOS was decreased in the hypoxia group while those of eNOS and nNOS were increased in the hypoxia group compared with the normoxia group. The expression of iNOS was increased in the resveratrol-treated group while those of eNOS and nNOS decreased in the resveratrol-treated group compared with a hypoxic group. CONCLUSION: The present study demonstrates resveratrol might affect nitric oxide synthases expression in HI injury of the perinatal period