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European Heart Journal Advance Access originally published online on July 24, 2006
European Heart Journal 2006 27(17):2054-2061; doi:10.1093/eurheartj/ehl154
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© The European Society of Cardiology 2006. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Prostacyclin improves transcoronary myocardial delivery of adipose tissue-derived stromal cells

Rosalinda Madonna1,2, Lucia Rinaldi1, Cosmo Rossi1, Yong-Jian Geng2 and Raffaele De Caterina1,3,*

1 Institute and Postgraduate School of Cardiology, G. d'Annunzio University—Chieti—Ospedale San Camillo de Lellis, Via C. Forlanini, 50, 66100 Chieti, Italy
2 University of Texas Health Science Center at Houston and Texas Heart Institute, Houston, TX, USA
3 CNR Institute of Clinical Physiology, Pisa, Italy

Received 28 February 2006; revised 8 June 2006; accepted 29 June 2006; online publish-ahead-of-print 24 July 2006.

* Corresponding author. Tel: +39 0871 41512; fax: +39 0871 553 461. E-mail address: rdecater{at}unich.it

Aims Heart transplantation of adipose tissue-derived stromal cells (ADSCs) is under evaluation as a therapy for cardiac repair. Prostacyclin (PGI2), a vasodilator with additional effects on platelet aggregation and blood cell adhesion, exerts cardioprotection and might favour the myocardial delivery of ADSCs. We investigated the engraftment and influence on cardiac function of the transcoronary delivery of ADSCs and the effects of PGI2 compared with nitroglycerin (NTG) and adenosine (Ado) in isolated–perfused mouse hearts.

Methods and results Infusion of ADSCs at <1x106 cells/mL caused no significant changes in contractility and rhythm, whereas higher cell doses caused cardiac dysfunction. Perfusion with PGI2, NTG, and Ado concentration-dependently increased coronary flow (CF). Perfusion with PGI2, at variance from NTG and Ado, increased ADSC delivery and entrance into the myocardial interstitium without affecting ventricular or metabolic functions and CF (engrafted ADSCs, as percentage of control, at doses producing 50% of maximum vasodilation: PGI2: 220±12, P<0.001; NTG: 110±8, P=N.S.; Ado: 80±5, P=N.S.).

Conclusion PGI2 safely increases myocardial delivery of ADSCs, by mechanisms independent of its vasodilatory properties, with a potential for its use in cell therapy for cardiac repair.

Key Words: Adipose tissue • Stem cells • Cell therapy • Prostacyclin • Cardiac repair • Coronary vasodilators


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