Glucose-insulin infusion improves cardiac function during fetal tachycardia
Michael Rahbek Schmidt, MD*,*,
Steen Buus Kristiansen, MD*,
Paul White, PhD ,
Morten Smerup, MD*,
Hans Erik Bøtker, MD, PhD*,
Michael Vogel, MD, PhD ,
Vibeke Hjortdal, MD, PhD, DMSc*,
Keld Sørensen, MD* and
Andrew Redington, MD, FRCP
* Aarhus University Hospital, Skejby Sygehus, Aarhus, Denmark
Papworth Hospital NHS Trust, Cambridge, Cambridgeshire, United Kingdom
Great Ormond Street Hospital for Sick Children, London, United Kingdom
Toronto Hospital for Sick Children, Toronto, Ontario, Canada

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Figure 1 Examples of changes in left ventricular dP/dt in a control (left panel) and a glucose-insulin-treated (right panel) isolated heart in the Langendorff preparation. There is a progressive fall in dP/dtmax and rise in dP/dtmin throughout the 90-min pacing protocol in the control heart.
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Figure 2 Box (in quartile range) and whisker (10th to 90th percentile) plot of systolic and diastolic performance of the isolated hearts in the control (left) and glucose-insulin (right) groups during 90 min of atrial pacing at 250 beats/min. Circles = outliers. LV = left ventricular.
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Figure 3 Comparison of free myocardial content of free glycogen (shown as nmol/mg wet weight biopsy) in control and glucose-insulin (GI) groups in the three lines of experiments. *p < 0.005; #p < 0.01. Solid bars = control; open bars = GI.
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Figure 4 Correlation between survival time and mean free myocardial glycogen content.
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Figure 5 Comparison of fetal and neonatal force-frequency relationships (see Results for details). LV = left ventricular.
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Figure 6 Individual fetal (in vivo) and neonatal systolic (dP/dtmax) and diastolic (tau) function during 90 min of pacing in controls (left panels) and glucose-insulin-treated (right panels) animals. Truncated curves illustrate premature death.
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