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Fetal cerebrovascular response to chronic hypoxia (CROSBI ID 508303)

Prilog sa skupa u zborniku | sažetak izlaganja sa skupa

Salihagić-Kadić, Aida ; Medić, Marijana ; Arbeille, Philippe Fetal cerebrovascular response to chronic hypoxia // Journal of Perinatal Medicine (Suppl). W de Gruyter, 2005

Podaci o odgovornosti

Salihagić-Kadić, Aida ; Medić, Marijana ; Arbeille, Philippe

engleski

Fetal cerebrovascular response to chronic hypoxia

Background: Cardiovascular adaptation to hypoxia is manifested by redistribution of blood flow primarily towards the fetal brain, which is most precisely detected by Doppler cerebro-umbilical ratio (C/U ratio = cerebral resistance index/umbilical resistance index). The aim of our studies was to explore the effects of chronic hypoxia on fetal cerebral circulation and to determine if long-term fetal brain hyperperfusion could be associated with brain lesions and adverse outcome. Methods and results: The effects of chronic hypoxia on cerebral circulation were studied on animal model and in two studies on human fetuses. Cerebro-umbilical ratio was determined in of 24 or 48 hours intervals, and results were interpreted according to the outcome parameters. In animal model, pregnant ewes were treated with cocaine (1 or 2mg/kg) daily from midgestation until delivery, resulting in significant fetal growth retardation and hypoxia. Acute hypoxic tests, performed prior to pregnancy termination, indicated reduced capability of brain vessels to vasodilate and heart rate to increase. In these animals, pathohistological examination revealed the existence of hypoxic brain lesions despite cerebrovascular reactivity. Five growth-retarded and hypoxic human fetuses were examined during 11-21 days prior to delivery. Blood flow redistribution with brain hyperperfusion was present from the beginning of the follow-up period. Early phase of fetal deterioration was characterized by progressive development of oligohydroamnios and disappearance of cerebrovascular reactivity. Fetal heart rate decelerations and increase in cerebral vascular resistance with brain hypoperfusion occurred 3-7 days after the loss of cerebrovascular reactivity. Decrease in C/U ratio and loss of cerebrovascular variability were associated with adverse fetal outcome, including fetal death (n=3). Histopathology of fetal brains revealed pathological gliosis and marked vasodilatation of cerebral arteries. In a prospective study, 29 growth-retarded human fetuses were followed during 15 days before delivery. Cerebro-umbilical ratio and new vascular score, hypoxia index (HI=change in C/U ratio (%<1) x duration in days) were tested as potential predictors of neonatal brain lesions. Brain lesions were detected ultrasonically in 13 hypoxic fetuses, and eight of them had a maintained cerebrovascular reactivity during whole observation period. Only HI was able to predict the development of perinatal brain lesions. Conclusion: During hypoxia, fetal blood flow redistribution towards the brain is followed by the loss of cerebrovascular reactivity and finally, with the increase in cerebral vascular resistance. Severe brain lesions can develop despite brain hyperpefusion and maintained vascular reactivity. New vascular score, HI would represent significant advance in prevention of hypoxic-ischemic brain lesions.

fetal hypoxia; doppler; brain lesions

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Podaci o prilogu

2005.

objavljeno

Podaci o matičnoj publikaciji

Journal of Perinatal Medicine (Suppl)

W de Gruyter

Podaci o skupu

Nepoznat skup

pozvano predavanje

29.02.1904-29.02.2096

Povezanost rada

nije evidentirano