title: Continuous measurement of ATP by 31P-NMR in term human dually perfused placenta in vitro: response to ischemia.
abstract: ATP was examined in dually perfused term human placentas by using 31P-nuclear magnetic resonance (NMR) spectroscopy. 31P-NMR spectra were acquired every 30 min starting approximately 30 min after establishing fetal and maternal perfusions, and maternal perfusate samples were obtained to monitor glucose utilization, lactate production, and human chorionic gonadotropin (hCG) and human placental lactogen (hPL) release. In continuous-perfusion experiments, placentas were perfused as long as 10 h. ATP increased and Pi fell after initiation of perfusion. Fetal volume loss was < 2 ml/h, and constant production of hCG, hPL, and lactate as well as constant utilization of glucose were observed. In additional experiments, ischemia was produced by halting maternal and fetal perfusion pumps after a 2-h control period. After 2, 3, or 4 h of ischemia, ATP decreased 46 +/- 17, 51 +/- 5, and 85% of control, respectively. When perfusion was reinitiated, ATP increased and was maintained for the duration of the experiment (an additional 2 h). Recovery of ATP after reperfusion was not paralleled by recovery in glucose utilization, lactate production, or hPL and hCG release. However, during the reperfusion period, fetal pressure was < 70 mmHg and fetal volume loss was < 2 ml/h. These investigations suggest that the dually perfused human placental lobule can maintain ATP for > or = 10 h. Although the perfused human placenta recovers ATP and maintains fetal perfusion volume after ischemia lasting up to 4 h, utilization of glucose, production of lactate, and production and release of hCG and hPL are impaired.
authors.affiliation: Department of Obstetrics and Gynecology, University of Rochester Medical Center, New York 14642, USA.
authors.forename: A
authors.initials: A
authors.lastname: Malek
authors.forename: R K
authors.initials: RK
authors.lastname: Miller
authors.forename: D R
authors.initials: DR
authors.lastname: Mattison
authors.forename: T
authors.initials: T
authors.lastname: Ceckler
authors.forename: M
authors.initials: M
authors.lastname: Panigel
authors.forename: P A
authors.initials: PA
authors.lastname: di Sant'Agnese
authors.forename: L N
authors.initials: LN
authors.lastname: Jessee
mesh_terms: D000255:Adenosine Triphosphate / Q000032:analysis / Q000378:metabolism*; D001786:Blood Glucose / Q000378:metabolism; D006063:Chorionic Gonadotropin / Q000378:metabolism; D005260:Female; D006801:Humans; D066298:In Vitro Techniques; D007511:Ischemia / Q000503:physiopathology; D007773:Lactates / Q000378:metabolism; D019344:Lactic Acid; D009682:Magnetic Resonance Spectroscopy; D010477:Perfusion; D010710:Phosphates / Q000378:metabolism; D010920:Placenta / Q000098:blood supply / Q000378:metabolism* / Q000502:physiology; D021041:Placental Circulation / Q000502:physiology*; D010928:Placental Lactogen / Q000378:metabolism; D011247:Pregnancy; D015424:Reperfusion
chemical_list: D001786:Blood Glucose; D006063:Chorionic Gonadotropin; D007773:Lactates; D010710:Phosphates; D019344:Lactic Acid; D000255:Adenosine Triphosphate; D010928:Placental Lactogen