6-ketoprostaglandin-f1-alpha and Birth-Weight

Very early human pregnancy is a state of cardiovascular underfilling. The renin-angiotensin system (RAS) is directly concerned with sodium and water homeostasis. Angiotensinogen is known to be the rate-limiting component in the generation of angiotensin I, and hence angiotensin II, in pregnancy. The usual measurement of 'renin activity' does not differentiate between enzyme and substrate. We hypothesized that the RAS is activated from the start of pregnancy; plasma renin concentration (PRC) and angiotensinogen will show differential regulation and might stimulate the rise in prostacyclin.. A prospective study of 12 nulliparous normal women. PRC and angiotensinogen and excretion of prostacyclin and thromboxane metabolites were measured pre-pregnancy and four to six times after conception to 13 weeks.. By 6 weeks gestation, mean PRC was markedly raised and remained stable to 13 weeks. The initial angiotensinogen response varied, but rose consistently after 6-8 weeks. Regression analysis showed angiotensinogen in the first trimester to be strongly associated with corrected birthweight centile (P < 0.001). Excretion of eicosanoid metabolites was very variable, but rose significantly from 6 weeks; the ratio between prostacyclin and thromboxane excretion did not alter over this time. There was no correlation between the various hormones measured.. Angiotensinogen is known to be rate-limiting in pregnancy. Its association with birthweight may be through effects on early plasma volume expansion and may have implications for intrauterine growth restriction and pre-eclampsia.

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Angiotensinogen; Birth Weight; Creatinine; Female; Humans; Longitudinal Studies; Pregnancy; Pregnancy Trimester, First; Prospective Studies; Renin; Renin-Angiotensin System; Thromboxane B2

Low endothelial generation of prostacyclin (PGI(2)) is a typical feature of pregnancy-induced hypertensive disorders. The aim of the current study was to establish whether changes in PGI(2) are accompanied by alterations in fetoplacental blood flow and to test the hypothesis that PGI(2) deficiency contributes to reduced fetoplacental perfusion in pregnancy-induced hypertension (PIH) and preeclampsia.. The study included 11 women with normal pregnancies, 12 with PIH/preeclampsia, and 7 with otherwise complicated pregnancies. Fetoplacental blood flow was assessed both by umbilical artery Doppler sonography measuring the resistance index (RI) and by means of neonatal birth weight. PGI(2) formation was measured in umbilical arteries prepared immediately after birth. PGI(2), RI and birth weight were correlated with and without correction for gestational age. Furthermore, data from patients with PIH/preeclampsia were compared with normal pregnancies as controls.. A significant inverse correlation was found between umbilical PGI(2) formation and umbilical RI and between birth weight and RI, whereas PGI(2) and birth weight were directly related. Patients with PIH/preeclampsia showed reduced PGI(2) formation, markedly increased gestational age-corrected RI and significantly reduced percentile birth weight.. These results provide evidence showing that PGI(2) is a relevant mediator of fetoplacental blood flow and suggest an important role of PGI(2) deficiency in PIH/preeclampsia.

Topics: 6-Ketoprostaglandin F1 alpha; Birth Weight; Epoprostenol; Female; Fetus; Gestational Age; Humans; Hypertension; Placenta; Pre-Eclampsia; Pregnancy; Pregnancy Complications, Cardiovascular; Ultrasonography; Umbilical Arteries; Vascular Resistance

To analyse whether pregnancies resulting in a small for gestational age neonate are preceded by a prostacyclin deficiency or an imbalance between thromboxane and prostacyclin.. At five fixed time points during pregnancy, 24-h urine samples were collected for the measurement of thromboxane and prostacyclin metabolites thromboxane-B(2) (TXB(2)) and 6-keto-prostaglandin F(1alpha) (6-keto-PGF(1alpha)). In order to study trend differences between pregnancies with appropriate (AGA; n=26) and small for gestational age neonates (SGA; n=17), trend analysis with simple contrasts were accomplished for TXB(2), 6-keto-PGF(1alpha) and the TXB(2)/6-keto-PGF(1alpha) ratio.. Trend analysis showed higher TXB(2) levels and higher TXB(2)/6-keto-PGF(1alpha) ratios in patients with SGA versus AGA newborns. No statistically significant difference in 6-keto-PGF(1alpha) excretion between patients with SGA and AGA newborns was detected.. The birth of an SGA neonate is not preceded by prostacyclin deficiency. With ongoing pregnancy an imbalance between thromboxane and prostacyclin becomes more obvious in pregnancies with SGA newborns.

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Birth Weight; Female; Gestational Age; Humans; Infant, Newborn; Infant, Small for Gestational Age; Pre-Eclampsia; Pregnancy; Thromboxane B2

Prostacyclin has a vasodilating effect on pulmonary vessels, whereas thromboxane A2 results in vasoconstriction. This study was designed to test the hypothesis that recurrent central apneas in preterm infants are correlated with a reduced prostacyclin to thromboxane A2 ratio. Twelve preterm infants with clinical events of apneas were matched with 12 control infants. Urinary concentration of 2,3-dinor-6-keto-PGF1alpha and 2,3-dinor-TxB2 was determined, and the ratio correlated with the number of central apneas (>20s) measured in overnight polygraphy. The number of central apneas >20s/12h was 97.4 (SE 7.8) in the study group, and 47.3 (SE 6.6) in the control group (p = 0.001). There was a significant correlation between the number of central apneas and the 2,3-dinor-6-keto-PGF1alpha/2,3-dinor-TxB2-ratio in all infants combined (r = -0.72, p < 0.0001) as well as in the two subject groups. Central apneas in premature infants are correlated with an decreased prostacyclin to thromboxane A2 ratio. The underlying pathomechanism may be increased intrapulmonary shunts with reflexive central apneas due to reduced pulmonary oxygenation.

Topics: 6-Ketoprostaglandin F1 alpha; Apnea; Birth Weight; Epoprostenol; Gestational Age; Humans; Infant, Newborn; Infant, Premature; Polysomnography; Prostaglandins F; Thromboxane A2; Thromboxane B2

Topics: 6-Ketoprostaglandin F1 alpha; Birth Weight; Cesarean Section; Female; Fetal Blood; Gestational Age; Humans; Labor, Obstetric; Maternal Age; Pregnancy; Prostaglandins F; Umbilical Arteries