Figure 2From: Characterization of mice with a deletion of protein kinase G type I in cardiomyocytes and the effect on cardioprotection through either postconditioning or mitochondria-targeted S-nitrosothiolResults of open chest experiments. As expected, either IPost, activation of sGC with BAY58 or A2BAR activation with BAY60 resulted in a profound decrease of infarct size in CMG-CTR. While BAY58 failed to protect in the CMG-KO animals, IPost, BAY60, and MitoSNO still afforded protection, suggesting a signaling independent on cGKI in the cardiomyocyte. *p<0.05 vs. control.Back to article page