(2)新生児脳障害に特異的な病態の解明とその予防および治療の可能性(シンポジウム3「新生児脳障害の減少に向けて」,<特集>第62回日本産科婦人科学会・学術講演会)

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  • The Specific Mechanisms for the Neonatal Encephalopathy and the Possibility for its Prevention and Treatment

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1. Using Seven-day-old neonatal hypoxia-ischemia rat model (Levine model), 1). We have shown the predominance of apoptotic cell death in the immature brain, and this cell death was significantly reduced by postischemic hypothermia. 2) We also have shown that hyperthermia during hypoxia-ischemia makes the immature brain inordinately susceptible to hypoxic-ischemic insult and causes brain injury, even if hypoxic-ischemic insult is so mild that it causes no or little injury by itself. This effect may also be mediated by the escalation of the apoptotic cell death pathway in the immature animal. 3). We also have shown that CTRX injections significantly enhanced GLT1 protein expression, and decreased hypoxic ischemic brain injury in the immature brain. 2. By use of a fluorescent O2 probe with a laser Doppler flowmeter in near-term fetal sheep, we measured values of cortical tissue O2 tension (tPO2), and laser Doppler cerebral blood flow (LD-CBF). Using this model, we have shown that 1). Maternal O2 administration significantly increased PaO2 and cerebral tPO2 of the fetus. 2). Hypercapnia favored cerebral tissue oxygenation of the fetal brain. 3). CO2 supplementation of maternal O2 administration enhanced fetal cerebral oxygenation. 4) Maternal caffeine administration significantly decreased cerebral oxygenation, without affecting systemic oxygenation. Using these animal models, we have investigated the specific mechanisms of the neonatal encephalopathy and the possibility of its prevention and treatment.

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