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Increased Platelet-activating Factor–acetylhydrolase Activity in the Umbilical Venous Plasma of Growth-restricted Fetuses

From the Department of Obstetrics and Gynecology, Kumamoto University School of Medicine, Kumamoto, and the Department of Obstetrics and Gynecology, Ehime University School of Medicine, Ehime, Japan.

Address reprint requests to: Toshihiro Yoshimura, MD Department of Obstetrics and Gynecology Kumamoto University School of Medicine Honjo 1-1-1, Kumamoto City Kumamoto 860-8556 Japan E-mail: yoshimur{at}kaiju.medic.kumamoto-u.ac.jp

Objective: To determine whether platelet-activating factor–acetylhydrolase activity in fetal plasma obtained at birth from umbilical vessels is different from that in maternal plasma, and (2) to compare platelet-activating factor–acetylhydrolase activity in cord plasma from fetuses with fetal growth restriction (FGR) and those with appropriate growth for gestational age (AGA).

Methods: Platelet-activating factor–acetylhydrolase activity was measured in the plasma of 22 nonpregnant healthy women, 16 pregnant women at term during labor, 28 fetuses exhibiting AGA, and seven fetuses with FGR.

Results: Plasma platelet-activating factor–acetylhydrolase activity in normotensive pregnant women at 37–41 weeks’ gestation was 28.1 ± 16.6 nmol/mL per minute, which was not statistically different from the activity in nonpregnant women (30.8 ± 11.1 nmol/mL per minute). Platelet-activating factor–acetylhydrolase activity in venous cord plasma from AGA fetuses was significantly (P < .01) lower than that in maternal plasma (6.3 ± 2.6 nmol/mL per minute), and there was no difference between the activities found in arterial and venous cord samples. In FGR fetuses, venous cord platelet-activating factor–acetylhydrolase activity was significantly (P < .01) higher (12.1 ± 1.4 nmol/mL per minute), than the activity seen in AGA fetuses, and when the data from AGA and FGR fetuses were considered together, there was a negative correlation between cord plasma platelet-activating factor–acetylhydrolase activity and neonatal body weight (r = .46, P = .006).

Conclusion: Platelet-activating factor hydrolysis is significantly lower in fetuses than adults. Further, the comparatively high platelet-activating factor–acetylhydrolase activity in FGR fetuses suggests the existence of a compensatory mechanism to maintain microcirculation within the placenta.

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