Intracoronary L-arginine during reperfusion improves endothelial function and reduces infarct size

Area of Science:

• Cardiovascular Research
• Ischemia-Reperfusion Injury
• Nitric Oxide Signaling

Background:

• Myocardial infarction leads to ischemia-reperfusion (I/R) injury.
• Nitric oxide (NO) plays a crucial role in cardiovascular homeostasis.
• L-arginine (L-Arg) is the physiological precursor for NO synthesis.

Purpose of the Study:

• To investigate if intracoronary L-Arg administration during reperfusion attenuates postischemic myocardial damage.
• To elucidate the role of L-Arg nitric oxide (NO) pathways in cardioprotection during I/R.

Main Methods:

• Open-chest dogs underwent 60 min LAD occlusion followed by 270 min reperfusion.
• Intracoronary administration of L-Arg, D-arginine (D-Arg), or saline vehicle (Veh) during early reperfusion.
• Infarct size, neutrophil accumulation (myeloperoxidase activity), and endothelial function were assessed.

Main Results:

• L-Arg significantly reduced infarct size (17.7%) compared to vehicle (34.8%).
• D-Arg reversed the cardioprotective effect of L-Arg (48.8%).
• L-Arg decreased neutrophil accumulation and preserved endothelial function in response to vasodilators.

Conclusions:

• Intracoronary L-Arg administration during early reperfusion reduces infarct size and neutrophil infiltration.
• L-Arg preserves endothelial function, likely via enhanced NO production.
• The L-Arg NO pathway is critical for mitigating I/R injury.