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用肺动脉环和全细胞膜片钳技术研究15-羟化二十烷四烯酸(15-HETE)对缺氧兔肺动脉平滑肌钾离子通道的影响。新出生的幼兔分两组,一组放入吸氧分数为0.12 的低氧舱内;另一组保持正常氧环境。9 d 后, 称重、取肺动脉进行细胞培养并制作肺动脉环。分别加入4-氨基吡啶(4-aminopyridione, 4-AP)、四乙胺(tetraethylammonium, TEA)、glyburide(GLYB)三种特异性钾离子通道阻断剂, 观察15-HETE 对兔肺动脉平滑肌钾离子通道的作用变化,同时采用全细胞膜片钳测定钾电流。结果显示: 5 mmol/L 4-AP 阻断KV通道后可以抑制15-HETE 诱导的缺氧兔肺动脉收缩;TEA和GLYB 分别阻断大电导型钙激活钾通道(BKCa)和KATP通道后并不影响15-HETE诱导的缺氧兔肺动脉收缩; 15-HETE可降低兔肺动脉平滑肌细胞钾电流幅度。上述结果提示: 缺氧兔肺动脉中,15-HETE阻断电压依赖钾通道(KV通道), 引起膜去极化, 可能是缺氧性肺血管收缩的机制之一。
Pulmonary artery rings and whole-cell patch-clamp technique were used to investigate the effect of 15-HETE on potassium channel in hypoxic rabbit pulmonary artery smooth muscle. Newborn rabbits divided into two groups, one group into the oxygen fraction of 0.12 oxygen chamber; the other group to maintain normal oxygen environment. After 9 days, the lungs were weighed, the pulmonary artery was taken for cell culture and the pulmonary artery rings were made. To investigate the effect of 15-HETE on potassium ion of pulmonary artery smooth muscle of rabbits, three specific potassium channel blockers, 4-aminopyridione (4-AP), tetraethylammonium (TEA) and glyburide (GLYB) The role of the channel changes, while using whole cell patch clamp determination of potassium current. The results showed that 5 mmol / L 4-AP block KV channels can inhibit 15-HETE induced hypoxic pulmonary arteries contraction; TEA and GLYB block large-conductance calcium-activated potassium channels (BKCa) and KATP channels, respectively 15-HETE can reduce the amplitude of potassium current in rabbit pulmonary artery smooth muscle cells. These results suggest that 15-HETE block the voltage-dependent potassium channels (KV channels) in hypoxic rabbit pulmonary arteries and cause membrane depolarization, which may be one of the mechanisms of hypoxic pulmonary vasoconstriction.