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Ann Thorac Surg 2001;72:1650-1656
© 2001 The Society of Thoracic Surgeons

Original article: cardiovascular

Insulin-like growth factor-1 improves postischemic recovery in hypertrophied hearts

Ingeborg Friehs, MDa, Christof Stamm, MDa, Hung Cao-Danh, PhDa, Francis X. McGowan, Jr, MDb, Pedro J. del Nido, MD*a

a Department of Cardiovascular Surgery, Children’s Hospital, Harvard Medical School, Boston, Massachusetts, USA
b Department of Anesthesiology/Critical Care, Children’s Hospital, Harvard Medical School, Boston, Massachusetts, USA

Accepted for publication June 29, 2001.

* Address reprint requests to Dr del Nido, Department of Cardiovascular Surgery, Children’s Hospital, Harvard Medical School, 300 Longwood Ave, Bader 279, Boston, MA 02115, USA
e-mail: pedro.delnido{at}tch.harvard.edu

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 (31P-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.




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