title: Metabolic acidosis decreases fetal myocardial isovolumic velocities in a chronic sheep model of increased placental vascular resistance.
abstract: We hypothesized that acute fetal metabolic acidosis decreases fetal myocardial motion in a chronic sheep model of increased placental vascular resistance (R(ua)). Eleven ewes and fetuses were instrumented at 118-122 days of gestation. After 5 days of recovery and 24 h of placental embolization to increase R(ua), longitudinal myocardial velocities of the right and left ventricles and interventricular septum (IVS) were assessed at the level of the atrioventricular valve annuli via tissue Doppler imaging (TDI). Ventricular inflow (E and A waves) and outflow velocities were obtained, and cardiac outputs were calculated. All measurements were performed at baseline and during fetal acidosis caused by epidural anesthesia-induced maternal hypotension, which decreased uterine artery volume blood flow, fetal oxygenation, arterial pH, and base excess and increased lactate. Compared with baseline, the peak isovolumic myocardial contraction and relaxation velocities of the ventricles and IVS, early relaxation velocity (E') of the ventricles, and systolic velocity of the IVS decreased during metabolic acidosis. The proportion of isovolumic contraction time of the cardiac cycle increased but the isovolumic relaxation and ejection time proportions and the TDI Tei index did not change. The E-to-E' ratio for both ventricles was higher during metabolic acidosis than at baseline. During metabolic acidosis, right and left ventricular cardiac outputs remained unchanged compared with baseline. In sheep fetuses with increased R(ua) and acute metabolic acidosis, global cardiac function was preserved. However, acute metabolic acidosis impaired myocardial contractility during the isovolumic phase and relaxation during the isovolumic and early filling phases of the cardiac cycle.
authors.affiliation: Department of Pediatrics, University of South Florida College of Medicine and All Children's Hospital, Children's Research Institute, 801 6th St. South, St. Petersburg, FL 33701, USA. ganesh.acharya@fagmed.uit.no
authors.forename: Ganesh
authors.initials: G
authors.lastname: Acharya
authors.forename: Juha
authors.initials: J
authors.lastname: Räsänen
authors.forename: Kaarin
authors.initials: K
authors.lastname: Mäkikallio
authors.forename: Tiina
authors.initials: T
authors.lastname: Erkinaro
authors.forename: Tomi
authors.initials: T
authors.lastname: Kavasmaa
authors.forename: Mervi
authors.initials: M
authors.lastname: Haapsamo
authors.forename: Luc
authors.initials: L
authors.lastname: Mertens
authors.forename: James C
authors.initials: JC
authors.lastname: Huhta
mesh_terms: D000138:Acidosis / Q000000981:diagnostic imaging / Q000378:metabolism / Q000503:physiopathology*; D000208:Acute Disease; D000818:Animals; D001794:Blood Pressure; D002302:Cardiac Output; D002496:Central Venous Pressure; D002908:Chronic Disease; D004195:Disease Models, Animal; D018619:Echocardiography, Doppler, Pulsed; D004621:Embolization, Therapeutic; D005260:Female; D005315:Fetal Diseases / Q000000981:diagnostic imaging / Q000378:metabolism / Q000503:physiopathology*; D005318:Fetal Heart / Q000000981:diagnostic imaging / Q000378:metabolism / Q000503:physiopathology*; D005865:Gestational Age; D006340:Heart Rate, Fetal; D006863:Hydrogen-Ion Concentration; D019344:Lactic Acid / Q000097:blood; D009200:Myocardial Contraction; D010100:Oxygen / Q000097:blood; D010920:Placenta / Q000098:blood supply*; D010927:Placental Insufficiency / Q000000981:diagnostic imaging / Q000378:metabolism / Q000503:physiopathology*; D011247:Pregnancy; D012107:Research Design; D012756:Sheep; D013997:Time Factors; D014655:Vascular Resistance; D016276:Ventricular Function
chemical_list: D019344:Lactic Acid; D010100:Oxygen