FP1-01RELATIONSHIP BETWEEN CEREBRALOXYGENATION <strong>AND</strong> PHOSPHORYLATIONPOTENTIAL DURING SECONDARY ENERGYFAILURE IN HYPOXIC-ISCHEMICNEWBORN PIGLETSTakashi Kusaka 1 , Masaaki Ueno 2 ,SaneyukiYasuda 3 ,Shinji Nakamura 4 ,Kosuke Koyano 5 , KenichiIsobe 6 ,Susumu Itoh 7Faculty of Medicine, Maternal and Perinatal Center, Kagawa University,Japan 1 ;Department of Pathology and Host Defense, Faculty of Medicine,Kagawa University, Japan 2 ; Faculty of Medicine, Maternal and PerinatalCenter, Kagawa Universit, Japany 3 ;Pediatrics, Faculty of medicine Kagawauniversity 4 , Pediatrics, Kagawa University, Japan 5,6,7The aim of this study was to evaluate the hypothesisthat cerebral hemoglobin (Hb) oxygenation is relatedto phosphorylation potential during primary andsecondary cerebral energy failure in newborn infantswho have experienced birth asphyxia. Wesubjected newborn piglets to severe transientcerebral hypoxic-ischemia followed by resuscitationand examined cerebral energy metabolism by31 P-magnetic resonance spectroscopy and evaluatedchanges in cerebral Hb oxygen saturation (ScO 2 )using full-spectrum near-infrared spectroscopy(NIRS) before, during, and up to 54 hours after thehypoxic-ischemic insult. ScO 2 was significantlydecreased during the hypoxic-ischemic insult ascompared to baseline values. During secondaryenergy failure, piglets were separated based on therelationship between the ratio of phosphocreatine toinorganic phosphate and ScO 2 ; those with a negativecorrelation were less injured than those with apositive correlation. These results indicate thatchanges in ScO 2 as measured by NIRS are related tophosphorylation potential during secondary energyfailure in newborn infants who have experiencedbirth asphyxia.This study is supported by Grants-in-Aid forScientific Research (C) nos. 19591281, 15591159,and (B) no. 17390307 from the Ministry ofEducation, Culture, Sports, Science, and Technologyof Japan.[Keywords]asphyxia, cerebral hemoglobin oxygen saturation,near-infrared spectroscopy, magnetic resonance spectroscopyFP1-02THE EFFECTS <strong>OF</strong> A SINGLE DOSEDEXAMETHASONE ON HIPPOCAMPALNEURONAL DEATH, <strong>AND</strong> ITS CORRELATIONTO NESTIN EXPRESSION IN RAT PUPSYung-Chieh Lin 1 , Tseng-Shian Tsai 2 , Chun-I Sze 3 , Yuh-JyhLin 4 , Chyi-Her Lin 5Pediatrics, National Cheng Kung University Hospita. Taiwanl 1, 4, 5 , Department ofPediatrics, National Cheng Kung University, Taiwan 2 , Department of Pathologyand Cell Biology and Anatomy, National Cheng Kung University, Taiwan 3BACKGROUND: Dexamethasone (Dex) has been used inpreterm infants for hypotension, and other purposes. However,Dex administration is associated with adverseneurodevelopmental outcomes. We reported that timing of Dexadministration is critical in causing apoptotic cell death in ratpup hippocampus. In this study, we hypothesized that neuralprecursors were prone to Dex- induced cell death inhippocampal formation in rat pups.OBJECTIVE: To investigate the effects of a single dose ofDex on neuroglial apoptotic cell death in hippocampalformation in rat pups.DESIGN/METHODS: Timed-dated Wistar Albino rat pupswere used. The pups were born at 21±1 gestational days (P-0)and litters were divided into two groups. The “Dex” groupreceived one dose of Dex (0.5 mg/kg) and the control receivedan equivalent volume of normal saline (NS) intraperitoneally onpostnatal day 1 (P-1); pups were killed after 24 hours, 48 hours,4 days, and 6 days. Brain tissues were processed. Five µmtissue sections were stained with TUNEL, immunofluorescence(IF), and immunohistochemical (IHC) methods. The levels ofproteins expression and the numbers of cells in proliferationand apoptotic cells were analyzed.RESULTS: IHC stains showed that levels of nestin, tubulin,and MAP2 expression decreased with the maturation of ratpups; the number of observed ki 67 stained cells, a cell markerin the cell cycle, increased in P-1 rat pups but continuallydecreased as rat pups matured. There was a trend in reductionof nestin protein expression in the control and Dex treated (P-1)groups. Double IF stains of nestin and TUNEL revealed that ahigher percentage of TUNEL-labeled cells were also expressingnestin (Control 61±3.3; Dex 75±3.7, n=6, p=0.01) in thehippocampus of P-1 group pups sacrificed 24 hrs after Dexinjection. TUNEL staining showed that P-1 Dex treated pupshad more cells undergoing apoptosis that the control. However,double IF staining of nestin with either caspase 3 or ki 67 didnot show any significant change in percentage of cellsco-expressing caspase 3 or ki 67 and nestin between the twogroups of pups.CONCLUSION: Twenty-four hours after injection, Dexenhances apoptotic cells in rat pup hippocampal formation;these cells have shown significant co-expression of nestin,which was not observed to be significant on double IF stains ofnestin with caspase 3 or ki 67. This suggests that Dex enhancesapoptotic cell death preferentially on cells maintaining thecharacteristics of neural precursor cells.[Keywords] Dexamethasone; neonatal brain injury; hippocampus ,animal model63
FP1-03BLUNTED CIRCADIAN RHYTHMS INHEART RATE <strong>OF</strong> SMALL FORGESTATIONAL AGE INFANTS IN EARLYNEONATAL PERIODBegum Esmot Ara 1 , Bonno Motoki 1, 2 , Sasaki Naoya 2 ,Omori Yusuke 2 , Sugino Noriko 2 , Yamamoto Hatsumi 1, 2National Hospital Organization, Miechuo Medical Center, ClinicalResearch Institute 1 and Department of Pediatrics and Neonatology 2 (Japan)OBJECTIVES: Small for gestational age (SGA) infants hasbeen documented for cardiovascular poor outcomes inneonatal and adult life. Circadian rhythm has been recognizedas a prognostic marker of cardiovascular health. However,little attention has been directed at the consequences of SGAto the circadian rhythmicity. The purpose of this study is toinvestigate the characteristics and consequences of circadianrhythmicity in SGA infants.METHODS: Twenty-four-hour heart rate was continuouslyrecorded by electrocardiogram during 0-2 postnatal days. Thestudy was conducted on a total of 156 infants; 39 infants wereSGA (birth weight and height bellow < -2SDs) and 117 wereappropriate for gestational age (AGA) infants (> -1.5 to
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