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目的：研究缺氧对大鼠大脑皮层神经元Ｌ型钙通道的影响和人参二醇皂苷（ＰＤＳ）保护的机制．方法：细胞贴附膜片钳法．结果：缺氧致钙通道开放时间由（２８５±０２１）ｍｓ增加到（９１±１０）ｍｓ（Ｐ＜００１），开放概率由（００４７±０００８）增加到（０１６５±００２５）（Ｐ＜００１）．ＰＤＳ（１５ｇ·Ｌ－１）抑制正常和缺氧时钙通道的开放［开放时间分别由（２２３±０４７）ｍｓ和（９１±１０）ｍｓ减到（１０３±０２５）ｍｓ和（２１±０４）ｍｓ，开放概率分别由（００４３±０００６）和（０１６５±００２５）减到（００１２±０００４）和（００２１±０００９）］．结论：缺氧可明显开放大鼠大脑皮层神经元Ｌ型钙通道，ＰＤＳ可有效抑制之，此为其保护缺氧脑的机制之一．
Objective: To study the effects of hypoxia on L-type calcium channels in rat cortical neurons and the mechanism of PDS protection. Methods: Cell patch patch clamp method. Results: The opening time of hypoxia induced calcium channel increased from (285±021)ms to (91±10)ms (P<001), and the open probability was (0047±0). 008) increase to (0165±0025) (P<001). PDS (15g·L-1) inhibits the opening of calcium channels during normal and hypoxia [open time from (223±047)ms and (91±10)ms] to (1) 03±025)ms and (21±04)ms, the open probability is reduced from (0043±0006) and (0165±0025) to (0012±) 0004) and (0021±0009)]. CONCLUSION: Hypoxia can significantly open up L-type calcium channels in rat cerebral cortical neurons. PDS can effectively inhibit it, which is one of the mechanisms of hypoxic brain protection.