L-Arginine ameliorates effects of ischemia and reperfusion in isolated cardiac myocytes.

We determined effects of the nitric oxide (NO) precursor L-arginine, on isolated guinea pig ventricular myocytes under normoxic conditions and simulated ischemia and reperfusion. Currents and contractions were recorded with voltage clamp and a video edge detector, respectively. In normoxia, L-arginine (50-200 microM) had little effect on Ca2+ current, but significantly decreased contraction. Ischemia in the absence of L-arginine reduced Ca2+ current and abolished contractions. In reperfusion, the arrhythmogenic transient inward current was induced and cells exhibited sustained contractile depression (stunning). With L-arginine (100 microM) in ischemia, Ca2+ current did not decline and recovery of contraction was potentiated in reperfusion. L-Arginine had no effect on transient inward current. Inhibition of nitric oxide synthase reversed effects of L-arginine on contractions but not Ca2+ current. Thus, NO contributes to beneficial effects of L-arginine in reperfusion, although effects on I(Ca-L) are independent of NO. Further, L-arginine effects differ under normoxic and ischemic conditions.