Decreased Prostacyclin Production: A Characteristic of Chronic Placental Insufficiency Syndromes

Prostacyclin-Like Activity in Umbilical Arteries Is Dose-Dependently Reduced by Maternal Smoking and Related to Nicotine Levels

“…cyanide, could also be of importance [24]. It is interesting to note that reduction of PGF production in umbilical vessels also has been reported to occur in syndromes with signs of chronic placental insufficiency, such as preeclampsia, essential hypertension and intrauterine growth retar dation [25]. In this study the exclusion of results from infants of mothers with pre eclampsia (two in each group) would not have altered the results.…”

Molecular Mechanisms Regulating the Vascular Prostacyclin Pathways and Their Adaptation during Pregnancy and in the Newborn

“…Studies in rat IUGR model induced by occlusion of uterine arteries during late pregnancy have shown increased maternal urinary levels of both 6-keto-PGF 1␣ and TXB 2 , but the elevation of both prostanoids seemed to originate from the uterus and not the placenta, which would lead to increased maternal systemic PGI 2 levels but may not translate into similar levels or effects in the placental circulation (Hophy et al, 1996). In humans, PGI 2 production was decreased in umbilical cord arteries of a small cohort of IUGR newborns born to mothers with chronic placental insufficiency and was related to chronic hypertension and PE or to unidentified cause (Stuart et al, 1981). However, in vitro, human placentas of severe IUGR pregnancies without hypertension produced similar or lower quantities of both PGI 2 and TXA 2 compared with controls, with no reduction in PGI 2 /TXA 2 ratio (Sorem and SilerKhodr, 1995).…”

“…In the absence of fetal genetic abnormalities, IUGR is often ascribed to placental insufficiency (Wareing et al, 2006), because it is often associated with extensive atherosclerotic and thrombotic lesions in the placental arteries and with placental infarction (Stuart et al, 1981). Placental oxidative stress, defective trophoblast invasion of arterioles, and RUPP similar to that seen in PE may be the underlying pathogenic mechanisms of both idiopathic IUGR and PE/IUGR pregnancies (Figueroa and Maulik, 2006;Karowicz-Bilinska et al, 2007).…”

Adrenomedullin in mammalian embryogenesis

“…The increased concentrations of AM in the circulation of IUGR fetuses are interpreted as a compensatory mechanism to the reduced uteroplacental flow caused by the altered production of other vasoactive agents, so that placental vascular resistance and/or fetal circulation would be maintained at physiologic levels (Di Iorio et al, 2000). For instance, levels of vasoactive molecules such as prostacyclin, nitric oxide, or atrial natriuretic peptide have also been reported to be altered in this type of pathology (Di Iorio et al, 1997a;Kingdom et al, 1992;Stuart et al, 1981), and AM could act as a paracrine regulator through the inhibition or stimulation of these factors. A correlation between umbilical AM concentrations in IUGR fetuses and the fetal cerebral/peripheral vessel ratio was also found; this fact suggested a potential role of AM in preferentially dilating cerebral vessels, in order to suppress the reduction of regional cerebral blood flow and prevent ischemic brain injury in IUGR (Di Iorio et al, 2000).…”