Journal
ANNALS OF THORACIC SURGERY
Volume 72, Issue 5, Pages 1650-1656Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/S0003-4975(01)03098-3
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Funding
- NHLBI NIH HHS [HL 52589, HL 63095] Funding Source: Medline
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Background. Severe myocardial hypertrophy is associated with decreased tolerance to ischemia compared with normal hearts. We hypothesized that treatment with insulin-like growth factor-1 (IGF-1) improves postischemic myocardial recovery by increasing glucose uptake during ischemia. and early reperfusion. Methods. Banding of the thoracic aorta in 10-day-old rabbits created pressure-overload hypertrophy. At 5 weeks of age (severe hypertrophy), aortic banded and sham-operated isolated hearts underwent 30 minutes of normothermic ischemia. with or without IGF-1 in the preischemic perfusate and cardioplegia. followed by 30 minutes of reperfusion. Results. 2-Deoxyglucose uptake (P-31-NMR) and phosphatidylinositol-3-kinase (PI-3-kinase) activity were significantly lower in hypertrophied hearts. Insulin-like growth factor-1 restored glucose uptake and PI-3-kinase activity to control levels in the hypertrophied hearts and both effects were blocked by wortmannin (a PI-3-kinase inhibitor). Postischemic developed pressure was significantly improved in IGF-1-treated hearts compared with untreated or IGF-1+wortmannin-treated hypertrophied hearts. Conclusions. These data indicate that IGF-1 improves glucose uptake and tolerance to ischemia in hypertrophied hearts. Myocardial IGF-1 effects are likely mediated through a PI-3-kinase-dependent pathway. (C) 2001 by The Society of Thoracic Surgeons.
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