胎児低酸素虚血性脳障害の予測から予防・治療へ : 過去の軌跡とこれからの可能性(第57回学術講演会講演要旨)

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Neonatal encephalopathy and its subset of hypoxic-ischemic encephalopathy (HIE) are conditions defined in and described for term and near-term infants. Epidemiologic studies have been shown that only 19% of cases of neonatal encephalopathy met what were very nonstringent criteria for intrapartum hypoxia, with another 10% experiencing a significant intrapartum event that may have been associated with intrapertum hypoxia. Thus, approximately 70% of neonatal encephalopathy is secondary to events arising before the onset of labor. Historically, the factors used to defined perinatal asphyxia were not specific to the disease process leading to neurological damage. Nelson et al. have shown that use of nonreassuring fetal heart rate patterns to predict subsequent cerebral palsy had a 99% false-positive rate. Severe perinatal asphyxia remains an important cause of brain injury in newborn infants, with a high risk for behavioral and neurological defects and death. At present, there have not been any treatments that are proven to be effective, and the emphasis thus far has been on supportive therapy. A potent neuroprotective effect of hypothermia following cerebral hypoxic ischemic injury has been reported in various animal models. Although several different models of neonatal cerebral hypoxia-ischemia (H-I) have been developed in the past, the modified Levene preparation in 7-day-old rats is the most commonly used model of cerebral H-I in immature animals. Using this model, postischemic hypothermia had a strong antiapoptotic effect leading to excellent neuroprotection. To investigate the effects of hypothermia on long-term neurofunctional outcome, we studied brainstem function using auditory brainstem response in adult rats after neonatal H-I brain injury. Hypothermia had an obvious inhibitory effect against caspase-3 activation and an excellent nuroprotective effect was observed 1 week after H-I. Postischemic hypothermia also provided effective and long-lasting neurofunctional as well as histopathologic protection to the immature brain. On the other hand, postischemic hyperthermia exacerbated H-I injury in immature brains, and the mechanism is strongly associated with activation of an apoptotic pathway. These results suggest that the body temperature is critical for perinatal H-I brain injury.
社団法人日本産科婦人科学会の論文
2005-08-01

胎児低酸素虚血性脳障害の予測から予防・治療へ : 過去の軌跡とこれからの可能性(第57回学術講演会講演要旨)

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