engleski

Could nitric oxide mediate hemodynamic response to fetal hypoxia in placeta.

INTRODUCTION When oxigen delivery to the fetus is compromised, certain circulatory and metabolic mechanisms will be activated. The fetal cardiovascular response to hypoxia is centralization of the blood flow to organs important for maintenance of fetal life such as 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. OBJECTIVE To investigate the role of nitric oxide (NO), a potent vasodilatator, 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 32 to 42 weeks of gestation. Doppler indices (CRI and URI) were measured at least twice and C/U was calculated. C/U less then 1, as a 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 of total supernatants of homogenized normal term placentas was 9, 47 +/- 1, 06 microMol/L (range 5, 98-16, 17 microMol/L). However, the same metabolites measured in samples of placentas from pregnancies with IUGR and hypoxia were statistically higher (p less than 0, 005) then normal, with mean value 52, 97 +/- 13, 06 microMol/L (range 25, 73+/-152, 74 microMol/L). CONCLUSION 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.

nije evidentirano

nije evidentirano