摘要
利用全细胞膜片箝方法研究间歇性低氧后左、右心室肌细胞短暂外向电流（Ｉｔｏ）的变化，以探讨间歇性低氧增强心肌电稳定性的离子机制。大鼠间歇性暴露于低氧环境２８ｄ（Ｈ２８，６ｈ／ｄ）后，右心室肌细胞的Ｉｔｏ密度较常氧对照组明显增加（１６１８±４６１比６３２±１３５ｐＡ／ｐＦ，Ｐ＜００５），而左心室肌细胞Ｉｔｏ密度与对照组无明显差异。间歇性低氧暴露４２ｄ（Ｈ４２）动物，其左、右心室肌细胞Ｉｔｏ密度与对照组无明显差异。Ｉｔｏ激活、失活和恢复动力学变化主要表现为Ｈ４２组左、右心室肌细胞的稳态失活曲线明显向负电压方向移位。左心室细胞的半数失活电压（－３８９±２３）ｍＶ与对照组（－３２８±５９）ｍＶ比较，具有显著性差异（Ｐ＜００１）；右心室细胞的半数失活电压（－４１９±４５）ｍＶ与对照组（－３３５±３５）ｍＶ比较，具有显著性差异（Ｐ＜０００１）。据此可推断，Ｉｔｏ密度的改变可反映心室在低氧早期阶段的不同动力学反应。
To explore the ionic basis of the strengthening effect of intermittent hypoxic adaptation (IHA)
on the electric stability of heart, the effects of intermittent hypoxia on the transient outward
current (Ito) in rat ventricular myocytes were investigated by using wholecell patchclamp
recording techniques. After 28day (H28) exposure (6 h/d)to intermittent hypoxia, the density of
Ito in the right, but not in the left, ventricular myocytes was dramatically increased as
compared with the normoxia control (1618461 vs 632135 pA/pF, P<005), while the Ito density
of the myocytes isolated from both sides of ventricles in 42dayexposure group (H42) did not
show significant difference. Except for a more negative shift of the steadystate inactivation
curves (halfinactivation voltages: -38923 vs -32859 mV in the left ventricle and -41945 vs
-33535 mV in the right ventricle) in the H42 group, all the other parameters for activation,
inactivation and recovery kinetics of Ito of each group remained unchanged. It is
speculated that the change in the current density of Ito may be responsible for the different
hemodynamic responses of the ventricles to the early stage of hypoxia. The alteration in
inactivation may participate in the cardioprotective effect of IHA.
出处
《生理学报》
CAS
CSCD
北大核心
1999年第2期187-188,共2页
Acta Physiologica Sinica
基金
国家自然科学基金
关键词
间歇性低氧
短暂外向电流
膜片箝技术
心肌缺血
intermittent hypoxia
transient outward current
patchclamp technique
adaptation
heart
