Exogenous B-type natriuretic peptide significantly limited infarct size in rat isolated hearts compared to control (20.1% vs 44.8%, P<0.01) via putative mitochondrial K(ATP) channel opening.
Does exogenous B-type natriuretic peptide reduce infarct size in isolated rat hearts undergoing ischemia-reperfusion?
Exogenous BNP limits myocardial infarct size in isolated rat hearts through a mechanism involving cGMP and mitochondrial K(ATP) channel opening.
Absolute Event Rate: 20.1% vs 44.8%
p-value: p=< 0.01
B-type natriuretic peptide (BNP) has been reported to be released from the myocardium during ischemia. We hypothesized that BNP mediates cardioprotection during ischemia-reperfusion and examined whether exogenous BNP limits myocardial infarction and the potential role of ATP-sensitive potassium (K(ATP)) channel opening. Langendorff-perfused rat hearts underwent 35 min of left coronary artery occlusion and 120 min of reperfusion. The control infarct-to-risk ratio was 44.8 +/- 4.4% (means +/- SE). BNP perfused 10 min before ischemia limited infarct size in a concentration-dependent manner, with maximal protection observed at 10(-8) M (infarct-to-risk ratio: 20.1 +/- 5.2%, P < 0.01 vs. control), associated with a 2.5-fold elevation of myocardial cGMP above the control value. To examine the role of K(ATP) channel opening, glibenclamide (10(-6) M), 5-hydroxydecanoate (5-HD; 10(-4) M), or HMR-1098 (10(-5) M) was coperfused with BNP (10(-8) M). Protection afforded by BNP was abolished by glibenclamide or 5-HD but not by HMR-1098, suggesting the involvement of putative mitochondrial but not sarcolemmal K(ATP) channel opening. We conclude that natriuretic peptide/cGMP/K(ATP) channel signaling may constitute an important injury-limiting mechanism in myocardium.
D’Souza et al. (Thu,) conducted a other in Myocardial infarction / ischemia-reperfusion injury. B-type natriuretic peptide (BNP) vs. Control was evaluated on Infarct-to-risk ratio (p=< 0.01). Exogenous B-type natriuretic peptide significantly limited infarct size in rat isolated hearts compared to control (20.1% vs 44.8%, P<0.01) via putative mitochondrial K(ATP) channel opening.