Naslov
Could nitric oxide mediate haemodynamic response to fetal hypoxia in placenta?

Autori
Tikvica, Ana ; Pintarić, Ivana ; Kušan Jukić, Marija ; Medić, Marijana ; Hudiček-Martinčić, Goranka ; Košec, Vesna ; Salihagić-Kadić, Aida

Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni

Skup
Zagreb International Medical Summit for Medical Students and Young Doctors

Mjesto i datum
Zagreb, Hrvatska, 26.10.2002. - 27.10.2002

Vrsta sudjelovanja
Poster

Vrsta recenzije
Nije recenziran

Ključne riječi
fetal hypoxia; intrauterine growth restriction; nitric oxide

Sažetak
Background: When oxygen delivery to the fetus is compromised, certain circulatory and metabolic mechanisms will be activated. The fetal cardiovascular responses to hypoxia are coordinated to centralize blood flow to organs important for maintenance of fetal life, such as the brain, heart and adrenals. The blood flow centralization, considered as one of the most important adaptive reactions, can be detected by Doppler ultrasound. The modifications of placental hemodynamics, responsible for fetal hypoxia, can be quantified by using the umbilical resistance index (URI), measured on the umbilical arterial Doppler velocity waveforms. The cerebrovascular adaptation (vasodilatation) can be assessed by using the cerebral resistance index (CRI), measured on the middle cerebral artery velocity waveforms. The flow redistribution between the placenta and the brain can be detected and quantified by using the cerebro-umbilical ratio (C/U). If any flow redistribution in favor of the brain occurs, the C/U ratio becomes less then 1. Moreover, it is the most sensitive parameter for the assessment of fetal growth retardation (IUGR) and fetal hypoxia. The aim of our study was to investigate the role of nitric oxide (NO), a potent vasodilator, in hemodynamic changes in placental insufficiency, IUGR and hypoxia, already detected by Doppler assessment. Study design and Results: The study included pregnant women with normal, in term delivery (n=12) and women with IUGR (n=10) from 33 to 40 weeks of gestation. Doppler indices (CRI and URI) were measured at least twice and C/U was calculated. C/U less then 1, as crucial parameter of fetal hypoxia and blood flow redistribution towards the brain, was recorded in all women with IUGR. After delivery the three samples from each placenta were collected and used for determination of NO metabolites (nitrate and nitrite) by Griese reaction. The mean total concentration of NO metabolites (nitrates and nitrites) measured in the supernatants of homogenized normal term placentas was 9.47 &plusmn ; ; 1.06 &micro ; ; Mol/L (range 5.98-16.17 &micro ; ; Mol/L). However, the same metabolites measured in samples of placentas from pregnancies with IUGR and hypoxia were statistically higher (p<0.005) than normal, with mean value 52.97 &plusmn ; ; 13.06 &micro ; ; Mol/L (range 25.73- 152.74 &micro ; ; Mol/L). Discussion and Conclusions: Our results suggest that the rather higher concentrations of NO metabolites in samples of placentas from pregnancies with IUGR and hypoxia implicate the activation of compensatory blood flow regulation mechanisms on the placental level. It means that the nitric oxide could be responsible for hemodynamic changes to hypoxia in placenta. Many other factors (drugs, nicotine, hormones) could be involved in induction of NO synthesis on the level of placenta during hemodynamic response to fetal hypoxia and their role also has to be considered.

Izvorni jezik
Engleski

Znanstvena područja
Kliničke medicinske znanosti

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