Vitamin C pretreatment attenuates hypoxia-induced disturbance of sodium currents in guinea pig ventricular myocytes.

As an important in vivo antioxidant, vitamin C is commonly used clinically to alleviate hypoxia-induced heart symptoms. To approach the protective mechanisms of vitamin C on hearts during hypoxia, we investigated the electrophysiological effects of vitamin C (1 mM: , pretreated before hypoxia) on Na(+) currents (including transient and persistent Na(+) currents) in guinea pig ventricular myocytes during hypoxia by the whole-cell and single-channel patch-clamp techniques. Whole-cell recordings showed that the mean current density of I (NaT) in the hypoxia group decreased from the control value of 40.2142 +/- 1.7735 to 27.1663 +/- 1.8441 pA/pF and current density of I (NaP) increased from 0.3987 +/- 0.0474 to 1.1854 +/- 01994 pA/pF (n = 9, P < 0.05 vs. control) at 15 min. However, when vitamin C was administered before hypoxia as pretreatment, I (NaT )and I (NaP )varied moderately (mean current density of I (NaT) decreasing from 41.6038 +/- 2.9762 to 34.6341 +/- 1.9651 pA/pF and current density of I (NaP) increasing from 0.3843 +/- 0.0636 to 0.6734 +/- 0.1057 pA/pF; n = 9, P < 0.05 vs. hypoxia group). Single-channel recordings (cell-patched) showed that the mean open probability and open time of I (NaP) increased significantly in both groups at hypoxia 15 min. However, the increased current values of the hypoxia group were still marked at hypoxia 15 min (n = 9, P < 0.05 vs. vitamin C + hypoxia group). Our results indicate that vitamin C can attenuate the disturbed effects of hypoxia on Na(+) currents (I (NaT) and I (NaP)) of cardiac myocytes in guinea pigs effectively.