title: Glucose-insulin infusion improves cardiac function during fetal tachycardia.
abstract: OBJECTIVE
  The aim of this work was to study the effects of substrate deficiency and supplementation on cardiac function during fetal tachycardia.
  
  
  BACKGROUND
  Although sustained fetal tachycardia may lead to cardiac failure and intrauterine death, neonatal tachycardia is generally better tolerated. Fetal myocardial energy production relies almost solely on glucose as substrate. We hypothesized that increased substrate availability by glucose-insulin (GI) infusion would improve fetal myocardial responses to tachycardia.
  
  
  METHODS
  We used three porcine models: 1) an isolated fetal heart model; 2) an in vivo fetal model; and 3) an in vivo closed-chest neonatal model. Each animal was randomized to control or GI treatment during tachycardia. In model 1, the controls were perfused with conventional Krebs-Henseleit solution containing a glucose concentration of 5.5 mmol/l; the GI hearts received double glucose concentration and added insulin. In models 2 and 3, the GI animals received insulin in a 20% glucose solution. All hearts were exposed to 90 min of pacing at 250 to 330 beats/min.
  
  
  RESULTS
  The isolated fetal hearts in the GI group showed no decline in dP/dt(max) during pacing, while the controls declined. In the in vivo fetal hearts, dP/dt(max) remained unchanged in the GI group and decreased significantly in the control group. Myocardial glycogen content was higher in the GI group than in controls. Functional indexes remained unchanged among both neonatal groups despite a higher glycogen content in the GI group.
  
  
  CONCLUSIONS
  Glucose-insulin infusion during fetal tachycardia has a beneficial effect on myocardial metabolism and cardiac function. These observations may have direct clinical relevance to the management of fetal arrhythmia.
authors.affiliation: Department of Cardiology, Research Unit, Aarhus University Hospital (Skejby), Skejby Sygehus, Brendstrupgaardsvej 100, DK-8200 Aarhus N, Denmark. rahbek@dadlnet.dk
authors.forename: Michael Rahbek
authors.initials: MR
authors.lastname: Schmidt
authors.forename: Steen Buus
authors.initials: SB
authors.lastname: Kristiansen
authors.forename: Paul
authors.initials: P
authors.lastname: White
authors.forename: Morten
authors.initials: M
authors.lastname: Smerup
authors.forename: Hans Erik
authors.initials: HE
authors.lastname: Bøtker
authors.forename: Michael
authors.initials: M
authors.lastname: Vogel
authors.forename: Vibeke
authors.initials: V
authors.lastname: Hjortdal
authors.forename: Keld
authors.initials: K
authors.lastname: Sørensen
authors.forename: Andrew
authors.initials: A
authors.lastname: Redington
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D004338:Drug Combinations; D005260:Female; D005315:Fetal Diseases / Q000188:drug therapy* / Q000378:metabolism; D005947:Glucose / Q000008:administration & dosage*; D006003:Glycogen / Q000378:metabolism; D007262:Infusions, Intravenous; D007328:Insulin / Q000008:administration & dosage*; D023421:Models, Animal; D010477:Perfusion / Q000379:methods; D011247:Pregnancy; D013552:Swine; D013610:Tachycardia / Q000188:drug therapy* / Q000378:metabolism; D016276:Ventricular Function / Q000187:drug effects* / Q000502:physiology
chemical_list: D004338:Drug Combinations; D007328:Insulin; D006003:Glycogen; D005947:Glucose