The aim of this study was to investigate the effect of hypoxia on the sodium current of rat cardiomyocytes in order to explore ion channel mechanism of cardiomyocyte hypoxia.The rat cardiomyocytes were isolated by acu...The aim of this study was to investigate the effect of hypoxia on the sodium current of rat cardiomyocytes in order to explore ion channel mechanism of cardiomyocyte hypoxia.The rat cardiomyocytes were isolated by acute enzymatic hydrolysis.A group of untreated cells were used to record sodium currents using whole-cell patch-clamp technique,another group was subjected to hypoxia and record sodium currents using same technique.The results showed that the morphological trajectory of sodium hypoxia was not changed compared with that of normal cells.The I-V curve of hypoxic cells was significantly higher than that of normal cells,and the peak current of INa was 15.68%higher than that of normal cells(P<0.0001).Activation potential of normal and hypoxia cells was about-40mV,the maximum peak current corresponds to the stimulation voltage of-25mV.The above results suggest that rat cardiomyocytes sodium current increases in the case of hypoxia.展开更多
The mechanism of idiopathic ventricular tachycardia originating from the right ventricular outflow tract （RVOT） is not clear. Many clinical reports have suggested a mechanism of triggered activity. However, there ar...The mechanism of idiopathic ventricular tachycardia originating from the right ventricular outflow tract （RVOT） is not clear. Many clinical reports have suggested a mechanism of triggered activity. However, there are few studies investigating this be- cause of the technical difficulties associated with examining this theory. The L-type calcium current （/Ca-L）, an important in- ward current of the action potential （AP）, plays an important role in arrhythmogenesis. The aim of this study was to explore differences in the APs of right ventricular （RV） and RVOT cardiomyocytes, and differences in electrophysiological character- istics of the ICa-L in these myocytes. Rabbit RVOT and RV myocytes were isolated and their AP and Ic,-L were investigated us- ing the patch-clamp technique. RVOT cardiomyocytes had a wider range of AP duration （APD） than RV cardiomyocytes, with some markedly prolonged APDs and markedly shortened APDs. The markedly shortened APDs in RVOT myocytes were abolished by treatment with 4-AP, an inhibitor of the transient outward potassium current, but the markedly prolonged APDs remained, with some myocytes with a long AP plateau not repolarizing to resting potential. In addition, early afterdepolariza- tion （EAD） and second plateau responses were seen in RVOT myocytes but not in RV myocytes. RVOT myocytes had a high- er current density for/Ca-L than RV myocytes （RVOT （13.16±0.87） pA pF-1, RV （8.59±1.97） pA pF-1; P〈0.05）. The ICa-L and the prolonged APD were reduced, and the EAD and second plateau response disappeared, after treatment with nifedipine （10 μmol L^-1）, which blocks the Ica-L. In conclusion, there was a wider range of APDs in RVOT myocytes than in RV myocytes, which is one of the basic factors involved in arrhythmogenesis. The higher current density for ICa-L is one of the factors causing prolongation of the APD in RVOT myocytes. The combination of EAD with prolonged APD may be one of the mechanisms of RVOT-VT generation.展开更多
文摘The aim of this study was to investigate the effect of hypoxia on the sodium current of rat cardiomyocytes in order to explore ion channel mechanism of cardiomyocyte hypoxia.The rat cardiomyocytes were isolated by acute enzymatic hydrolysis.A group of untreated cells were used to record sodium currents using whole-cell patch-clamp technique,another group was subjected to hypoxia and record sodium currents using same technique.The results showed that the morphological trajectory of sodium hypoxia was not changed compared with that of normal cells.The I-V curve of hypoxic cells was significantly higher than that of normal cells,and the peak current of INa was 15.68%higher than that of normal cells(P<0.0001).Activation potential of normal and hypoxia cells was about-40mV,the maximum peak current corresponds to the stimulation voltage of-25mV.The above results suggest that rat cardiomyocytes sodium current increases in the case of hypoxia.
文摘The mechanism of idiopathic ventricular tachycardia originating from the right ventricular outflow tract （RVOT） is not clear. Many clinical reports have suggested a mechanism of triggered activity. However, there are few studies investigating this be- cause of the technical difficulties associated with examining this theory. The L-type calcium current （/Ca-L）, an important in- ward current of the action potential （AP）, plays an important role in arrhythmogenesis. The aim of this study was to explore differences in the APs of right ventricular （RV） and RVOT cardiomyocytes, and differences in electrophysiological character- istics of the ICa-L in these myocytes. Rabbit RVOT and RV myocytes were isolated and their AP and Ic,-L were investigated us- ing the patch-clamp technique. RVOT cardiomyocytes had a wider range of AP duration （APD） than RV cardiomyocytes, with some markedly prolonged APDs and markedly shortened APDs. The markedly shortened APDs in RVOT myocytes were abolished by treatment with 4-AP, an inhibitor of the transient outward potassium current, but the markedly prolonged APDs remained, with some myocytes with a long AP plateau not repolarizing to resting potential. In addition, early afterdepolariza- tion （EAD） and second plateau responses were seen in RVOT myocytes but not in RV myocytes. RVOT myocytes had a high- er current density for/Ca-L than RV myocytes （RVOT （13.16±0.87） pA pF-1, RV （8.59±1.97） pA pF-1; P〈0.05）. The ICa-L and the prolonged APD were reduced, and the EAD and second plateau response disappeared, after treatment with nifedipine （10 μmol L^-1）, which blocks the Ica-L. In conclusion, there was a wider range of APDs in RVOT myocytes than in RV myocytes, which is one of the basic factors involved in arrhythmogenesis. The higher current density for ICa-L is one of the factors causing prolongation of the APD in RVOT myocytes. The combination of EAD with prolonged APD may be one of the mechanisms of RVOT-VT generation.
