Pregled bibliografske jedinice broj: 317729
Fetal cerebrovascular response to chronic hypoxia-implications for the prevention of brain damage
Fetal cerebrovascular response to chronic hypoxia-implications for the prevention of brain damage // Periodicum Biologorum-Suppl. 2
Zagreb, 2007. (pozvano predavanje, domaća recenzija, sažetak, znanstveni)
CROSBI ID: 317729 Za ispravke kontaktirajte CROSBI podršku putem web obrasca
Naslov
Fetal cerebrovascular response to chronic hypoxia-implications for the prevention of brain damage
Autori
Salihagić-Kadić, Aida ; Arbeille, Philippe
Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni
Izvornik
Periodicum Biologorum-Suppl. 2
/ - Zagreb, 2007
Skup
5. Hrvatski kongres farmakologije i 2. kongres Hrvatskog društva fiziologa s međunarodnim sudjelovanjem
Mjesto i datum
Osijek, Hrvatska, 19.09.2007. - 22.09.2007
Vrsta sudjelovanja
Pozvano predavanje
Vrsta recenzije
Domaća recenzija
Ključne riječi
fetal hypoxia; brain lesions
Sažetak
Introduction: Fetal cardiovascular responses to hypoxia, which include the redistribution of the cardiac output towards the vital organs, are considered the most important adaptive reactions responsible for maintaining fetal homeostasis. The redistribution of blood flow towards the fetal brain is known as « ; the brain sparing effect» ; and it can be precisely detected and quantified by the Doppler cerebral/umbilical ratio (C/U ratio = cerebral resistance index (CRI) /umbilical resistance index (URI)). Objectives: 1. to investigate the effects of chronic hypoxia on fetal cerebral circulation, 2. to determine whether prolonged fetal brain hyperperfusion (the brain sparing effect) is associated with the brain damage and a poor fetal outcome, 3. to estimate the value of the new vascular score, the hypoxia index in the prediction of brain lesions caused by fetal hypoxia. Material and Methods: Fetal cerebrovascular response to hypoxia were studied on an animal model and on human fetuses. In the animal model, pregnant ewes (n=14) were treated with cocaine (1 or 2 mg/kg) daily from midgestation until delivery, resulting in a significant fetal growth retardation and chronic hypoxia. The control group (n=7) received placebo injected intramuscularly daily in the same period. Cerebral flow responses and heart rate were measured at rest and during two acute hypoxic tests (cord compression and maternal aorta compression) at the cesarean delivery perfomed on day 134. In a prospective study, 29 growth-restricted and hypoxic human fetuses (29-38 weeks of gestation) were followed at least two weeks prior to delivery. The C/U ratio was determined in 48 hours intervals and the hypoxia index (HI) was calculated by summing the daily C/U ratio reduction (in % from the cut-off value of 1) over the period of observation. The C/U ratio and the HI were tested as potential predictors of the neonatal brain damage. Neonatal brain sonography and perinatal data were used as the outcome parameters. Results: Long-term exposure to cocaine induces the redistribution of blood floow towards the brain. During the hypoxic tests, the CRI and the C/U ratio decreased significantly less in the two cocaine groups (p<0.05). The fetal heart rate response was reduced significantly in the two cocaine groups (p<0.05). Pathohistological examination revealed the existence of hypoxic brain damage despite the maintained cerebrovascular reactivity and the brain sparing effect. During the period of surveillance of the human fetuses, hypoxia was detected in 22 fetuses and the neonatal brain damage were later found in 13 of these infants. In five hypoxic fetuses, cerebrovascular variability was lost for a minimum period of six days and the brain damage were later detected in all of them. Neonatal brain damage were also detected in eight hypoxic fetuses with the maintained cerebrovascular variability. The HI was identified as a predictor of the neonatal brain damage. The HI also showed the best correlation with biochemical parameters, such as umbilical venous pO2 (r=-0.60, p<0.001) and umbilical venous pH (r=-0.66, p<0.001). Conclusion: Our studies have demonstrated clearly that the brain sparing effect cannot prevent the development of perinatal brain damage in the case of severe or prolonged hypoxia. Brain damage can develop even before the loss of physiological cerebrovascular variability. The use of HI could allow for the first time a sensitive and reliable prediction and even the prevention of adverse neurological outcome in pregnancies complicated by hypoxia.
Izvorni jezik
Engleski
Znanstvena područja
Temeljne medicinske znanosti, Kliničke medicinske znanosti
POVEZANOST RADA
Projekti:
108-1081870-1940 - C/U omjer i motorički parametri u prevenciji perinatalnog oštećenja mozga (Salihagić-Kadić, Aida, MZOS ) ( CroRIS)
Ustanove:
Medicinski fakultet, Zagreb
Profili:
Aida Salihagić
(autor)
Citiraj ovu publikaciju:
Časopis indeksira:
- Web of Science Core Collection (WoSCC)
- Science Citation Index Expanded (SCI-EXP)
- SCI-EXP, SSCI i/ili A&HCI
- Scopus