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Am J Physiol Heart Circ Physiol 279: H260-H268, 2000;
0363-6135/00 $5.00
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Vol. 279, Issue 1, H260-H268, July 2000

Basic FGF reduces stunning via a NOS2-dependent pathway in coronary-perfused mouse hearts

Thomas G. Hampton1, Ivo Amende1,2, Jason Fong1, Victor E. Laubach3, Jian Li1,4, Carolyn Metais4, and Michael Simons1,4

1 Cardiovascular Division and 4 Angiogenesis Research Center, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215; 2 Department of Cardiology, Medical University, D-30625 Hannover, Germany; and 3 Department of Surgery University of Virginia Health Sciences Center, Charlottesville, Virginia 22908

Basic fibroblast growth factor (FGF-2) may protect the heart from ischemia-reperfusion injury (stunning) by stimulating nitric oxide (NO) production. To test this hypothesis, we pretreated coronary-perfused mouse hearts with 1 µg/ml FGF-2 or vehicle control before the onset of ischemia. Intracellular calcium (Cai2+) was estimated by aequorin, and NO release was measured with an NO-selective electrode. Hearts perfused with FGF-2 maintained significantly better left ventricular (LV) function during ischemia than hearts perfused with vehicle. FGF-2 significantly delayed the onset of ischemic contracture and improved LV recovery during reperfusion. Cai2+ was similar in both groups at baseline during ischemia and reperfusion. L-N6-(1-iminoethyl)lysine, a selective inhibitor of inducible NO synthase (NOS2), obliterated the protective effects of FGF-2. In transgenic hearts deficient in the expression of NOS2 (NOS2-/-), FGF-2 did not attenuate ischemia-induced LV dysfunction. Measurements of NO release demonstrated that FGF-2 perfusion significantly increased NO in wild-type but not in NOS2-/- hearts. We conclude that basic FGF attenuates myocardial stunning independent of alterations in Cai2+ by stimulating NO production via an NOS2-dependent pathway.

ischemia; nitric oxide; intracellular calcium; myocardial function


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