| First Author | Hampton TG | Year | 2000 |
| Journal | Am J Physiol Heart Circ Physiol | Volume | 279 |
| Issue | 1 | Pages | H260-8 |
| PubMed ID | 10899065 | Mgi Jnum | J:107850 |
| Mgi Id | MGI:3622379 | Doi | 10.1152/ajpheart.2000.279.1.H260 |
| Citation | Hampton TG, et al. (2000) Basic FGF reduces stunning via a NOS2-dependent pathway in coronary-perfused mouse hearts. Am J Physiol Heart Circ Physiol 279(1):H260-8 |
| abstractText | 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 microg/ml FGF-2 or vehicle control before the onset of ischemia. Intracellular calcium (Ca(i)(2+)) 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. Ca(i)(2+) was similar in both groups at baseline during ischemia and reperfusion. L-N(6)-(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 Ca(i)(2+) by stimulating NO production via an NOS2-dependent pathway. |
