Figure 4.

Effect of NO release, as measured by nitrite $\left({\text{NO}}_2^{-}\right)$ levels in vehicle- and NOS inhibitor-treated NTg and FGF2 Tg hearts. Nitrite release was significantly elevated in FGF2 Tg hearts compared to NTg hearts. L-NAME treatment resulted in a decreased level of nitrite release FGF2 Tg hearts, indicating that NOS activity was inhibited (A), L-NIL treatment (B) or TRIM administration (C) resulted in a decreased level of nitrite release in FGF2 Tg hearts, indicating that NOS activity was inhibited and that iNOS and/or nNOS activity was important for NO production leading to protection against I-R injury. NTg, + black triangle; NTg + L-NAME, open triangle; NTg + L-NIL, open triangle/dashed line; NTg + TRIM, open triangle/gray dashed line; FGF2 Tg, black square; FGF2 Tg + L-NAME, open square; FGF2 Tg + L-NIL, open square/dashed line; and FGF2 Tg + TRIM, open square/gray dashed line. Gray region, time points of inhibitor treatment (15 min prior to through first 15 min of ischemia and last 15 min of ischemia through first 15 min of reperfusion). n = 11–15 hearts per group. *p < 0.05 vs. NTg from same treatment. #p < 0.05 vs. FGF2 Tg NOS inhibitor treatment.