{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,14]],"date-time":"2026-01-14T17:52:15Z","timestamp":1768413135492,"version":"3.49.0"},"reference-count":48,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2012,4,11]],"date-time":"2012-04-11T00:00:00Z","timestamp":1334102400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Prenatal Diagnosis"],"published-print":{"date-parts":[[2012,5]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:sec><jats:title>Objective<\/jats:title><jats:p>The authors aimed to study the contractility responses of normal and fetal growth restriction (FGR) placentas to prostaglandin E<jats:sub>2<\/jats:sub> (PGE<jats:sub>2<\/jats:sub>) and to correlate the results to subsequent placental histological analysis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Method<\/jats:title><jats:p>A dual\u2010perfused single cotyledon model was used. Placentas from pregnancies complicated by FGR and from normal pregnancies were obtained. Selected cotyledons were cannulated and dually perfused. Following stabilization, three concentrations of PGE<jats:sub>2<\/jats:sub> (0.05, 0.1, and 0.15\u2009mg\/mL) were administered to the fetal arterial side causing contraction\/relaxation response. Fetal perfusion pressure was measured continuously during these contraction and relaxation phases. Following the perfusion experiments, the placentas were analyzed for fetal or maternal origin vascular lesions.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>A total of 21 complete experiments were performed (16 normal, 5 FGR). In response to PGE<jats:sub>2<\/jats:sub>, FGR placentas exhibited lower change in the perfusion pressure and lower relaxation time constant. Basal perfusion pressure did not differ significantly between the two groups. Placental histopathology lesions, fetal or maternal origin, were more common in the FGR compared with the controls placentas, 80% versus 25%, respectively, <jats:italic>P<\/jats:italic>\u2009=\u20090.047.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>The lower vascular reactivity in response to PGE<jats:sub>2<\/jats:sub> and the presence of fetal and maternal vascular placental lesions suggest a mechanism explaining the altered vascular supply in FGR. \u00a9 2012 John Wiley &amp; Sons, Ltd.<\/jats:p><\/jats:sec>","DOI":"10.1002\/pd.3827","type":"journal-article","created":{"date-parts":[[2012,4,12]],"date-time":"2012-04-12T03:13:24Z","timestamp":1334200404000},"page":"417-422","source":"Crossref","is-referenced-by-count":10,"title":["Reactivity of blood vessels in response to prostaglandin E<sub>2<\/sub> in placentas from pregnancies complicated by fetal growth 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