Figure 2.

Myocardial PKA activity and the expression of Ser¹³³ p-CREB, eNOS and p-eNOS (Ser¹¹⁷⁹ and Ser⁶³⁵) after ischemia and reperfusion. (A) Myocardial PKA activities in the reflow and no-reflow areas were stimulated by ischemia and reperfusion and were further increased by SIM pretreatment. However, the SIM-induced activation of PKA was silenced by H-89 but not by L-NNA. (B) In the non-ischemic area, the expression of eNOS and Ser⁶³⁵ p-eNOS was increased in the control group, and the expression of Ser¹³³ p-CREB and eNOS was decreased in the SIM and H-89 groups. (C) In the reflow area, the expression of Ser¹³³ p-CREB, eNOS, and Ser⁶³⁵ p-eNOS was stimulated by ischemia and reperfusion. SIM promoted the phosphorylation of Ser¹³³ p-CREB, Ser¹¹⁷⁹ p-eNOS, and Ser⁶³⁵ p-eNOS. However, H-89 counteracted the effects of SIM on Ser¹³³ p-CREB and Ser⁶³⁵ p-eNOS, and L-NNA canceled the effects of SIM on Ser¹¹⁷⁹ p-eNOS and Ser⁶³⁵ p-eNOS. (D) In the no-reflow area, ischemia and reperfusion induced the phosphorylation of Ser¹³³ p-CREB and Ser¹¹⁷⁹ p-eNOS. SIM pretreatment increased the phosphorylation of Ser¹³³ p-CREB and Ser⁶³⁵ p-eNOS. H-89 blocked the effect of SIM on Ser¹³³ p-CREB, and L-NNA inhibited the SIM effects on Ser¹¹⁷⁹ p-eNOS and Ser⁶³⁵ p-eNOS. Mean±SEM. n=7–8 animals/group. ^bP<0.05 vs Sham. ^eP<0.05 vs Control. ^hP<0.05, ⁱP<0.01 vs SIM at the same time point.