Effect of Vitamin E on Cerebral Hypoxia-Ischemia in Neonatal Rats

PURPOSE: In order to evaluate the hypoxia-ischemia induced neurotoxic effect and the protective effect of vitamin E as an antioxidant, cell number and cell viability were measured in cerebral neurons and astrocytes derived in neonatal rats. METHODS: 7-day old neonatal rats were subjected to unilateral common carotid artery occlusion, and exposed to hypoxic condition for 3 hours. The protective effect of vitamin E, as an antioxidant was examined by XTT [2,3-bis(2-methoxy-4-nitro-5-sulfophenyl)-5-(phenylami-nocarbonyl) 12H-tetrazolium hydroxide] assay and cell number on 14 days after hypoxia-ischemia when the rats received an intraperitoneal injection of vitamin E immediately following hypoxia-ischemia. RESULTS: Hypoxic-ischemic condition positively decreased the cell number and cell viability of rat cerebral neurons in a time-dependent manner when rats were killed 72 hours after hypoxia- ischemia. 72 hours after hypoxia-ischemia, the cell number and viability of astrocytes were slightly decreased, compared with the saline treated group. In rats treated with vitamin E, the cell number and cell viability of neurons were significantly increased compared with those of the saline- or non-treated group. In hypoxic-ischemic treated rats after 14 days from hypoxia- ischemia, astrocytes were significantly proliferated, but vitamin E showed the protective effect on hypoxic-ischemia induced cell proliferation and cell viability. CONCLUSION: It is suggested that hypoxic-ischemic condition is more toxic in neurons than astrocytes, and selective antioxidants such as vitamin E, especially when it was administered within two hours after hypoxia-ischemia, is highly effective in preventing the cell death of neurons and astrocytes from hypoxia-ischemic condition in neonatal rats.

Cytotoxicity of Diamide and the Protective Effect of Thioredoxin on Diamide-Induced Vasculotoxicity in Vascular Endothelial Cells

BACKGROUND AND OBJECTIVES: This study was designed to examine the effects of diamide and thioredoxin (TRX) on vascular endothelial cells in order to clarify the mechanism by which vascular damage is mediated by oxygen free radicals. MATERIALS AND METHODS: The pulmonary artery endothelial cell (PAEC) line derived from bovine serum was cultured for 8 hours in media supplemented with various concentrations of diamide and TRX. The XTT assay, MTS assay, SRB assay, LDH activity and lipid peroxidation tests were perfomed. RESULTS: In XTT and MTS assays, diamide significantly decreased the cell viability of cultured PAEC in a dose- and time-dependent manner. Diamide showed a decrease in the amount of total protein, although it showed an increase of lipid peroxidation and LDH activity in cultured PAEC. In regards to the protective effect of TRX on diamide-induced cytotoxicity, this showed an increase of total protein, however it showed a decrease of lipid peroxidation and LDH activity. CONCLUSION: Our results suggest that diamide has a vasculotoxic effect on cultured bovine PAEC and that TRX is very effective in the protection of diamide-induced cytotoxicity by duye to the increase of total protein and the decrease of lipid peroxidation and LDH activity in these cultures.

Effect of Body Position on Gastric Emptying / 대한주산의학회잡지

No abstract available.

A Case of Matemal Hemorrhage

Fetomaternal hemorrhage is very common and the commonest cause of anernia in the newborn. But, few blood cells enter the maternal circulation in most pregnancies. Occasionally large intrauterine bleeding results in severe fetal and neonatal anemia, shock, and rarely death. To identify the fetal blood in the maternal circu1ation, acid elution technique of Kleihauer-Betke test is usually used. And imrnedate neonatal blood transfusion should be done for good prognosis. We report a case of massive feto-maternal hemorrhage (>100 ml) in a preterm neonate with severe anemia at birth, which was diagnosed by Kleihauer-Betke test and was treated with blood transfusion.