Objectives: 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.