Key result
Postconditioning reduced infarct size to 22% of the risk area compared to 61% in control hearts (p<0.01), an effect mediated by intermittent bradykinin B2 receptor and mKATP channel activation.
Population
Isolated rat hearts undergoing 30 min ischemia and 120 min reperfusion
Comparison
Postconditioning, intermittent bradykinin… vs Control hearts
Design
Preclinical
Follow-up
120 min reperfusion
Authors
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Postconditioning cardioprotection remains preclinical; leaves open translation of B2 receptor or mKATP targeting to human reperfusion injury.
Absolute Event Rate: 22% vs 61%
p-value: p=<0.01
Intermittent targeting of bradykinin B2 receptors and mitochondrial KATP channels during early reperfusion triggers postconditioning protection via ROS signaling in isolated rat hearts.
Penna et al. (2007) studied Ischemia/reperfusion injury. Postconditioning (PostC) or Intermittent bradykinin (BK) infusion vs. Control was evaluated on Infarct size (% of risk area) (p=<0.01). Postconditioning reduced infarct size to 22% of the risk area compared to 61% in control hearts (p<0.01), an effect mediated by intermittent bradykinin B2 receptor and mKATP channel activation.
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