ABSTRACT
AIM:To observe the effects of granulocyte colony-stimulating factor (G-CSF) on calcium, sodium and potassium ion channel currents of the ischemic atrial myocytes in guinea pig by whole-cell patch clamp technique.METHODS:The guinea pig atrial myocytes were obtained by enzymolysis.Under ischemia and hypoxia condition, whole-cell patch clamp was used to observe the effects of G-CSF at various concentrations on the changes of the I-V curve, activation curve and availability of L-type calcium channel current (ICa,L) and voltage-dependent sodium channel current (INa), as well as I-V curve of delayed rectifier potassium channel current (IK).RESULTS:Under ischemic condition, the I-V curves of ICa,L were changed by acute G-CSF intervention in a dose-dependent fashion.Except for G-CSF at dose of 300 μg/kg, the other concentrations of G-CSF did not change the activation curve and availability of ICa,L, indicating that the effects of G-CSF on ICa,L were in a voltage-independent fashion.The I-V curves of ICa,L under ischemic condition were gradually approaching the normal levels by the higher dose of G-CSF, while the effect of 300 μg/kg G-CSF on ICa,L was similar to 100 μg/kg G-CSF.Acute G-CSF intervention at different doses did not change I-V curve, activation curve, and availability or steady-state availability of INa.As a part of IK, the rapid activating component (IKr) was improved by 100 μg/kg and 300 μg/kg G-CSF intervention with the similar effects, while the slowly activating component (IKs) was not changed by G-CSF.CONCLUSION:G-CSF affects ion channel electrophysiological properties of ischemic atrial myocytes in a voltage-independent but concentration-dependent manner, thus reducing the incidence of atrial arrhythmia.
ABSTRACT
Objective To investigate the effects of midazolam on the delayed rectifier outward potassium channel current (Ik) using the whole-cell patch clamp technique. Methods Pyramidal neurons were isolated acutely from 5-15 d SD rat hippocampus. We measured amplitudes of the delayed outward rectifier potassium currents by activating depolarizing pulse from - 50mV to 30mV. Different concentrations of midazolam were added and potassium channel currents were measured. Results Delayed outward rectifier potassium channel currents were inhibited by midazolam in a dose-dependent manner. EC50 was (8.31 ?2.78) ? 10-8 mol/L and Hill constant was 0.90? 0.16.Conclusions Our results suggest that block of the outward rectifier potassium channel current by midazolam may contribute to the mechanism of midazolam anesthesia action.