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.