左旋硝基精氨酸对缺氧加强氯化钾收缩离体猪冠状动脉的影响

EFFECTS OF NITRO-L-ARGININE ON HYPOXIA-POTENTIATED KCL-INDUCED CONTRACTION OF THE ISOLATED PORCINE CORONARY ARTERY

左旋硝基精氨酸（Ｎｉｔｒｏ－Ｌ－Ａｒｓｉｎｉｎｅ，ＮＬＡ）２００μｍｏｌ／Ｌ几乎阻断缺氧加强氯化钾（２０ｍｍｏｌ／Ｌ）收缩离休猪冠状动脉的作用，并可轻度加强氯化钾收缩反应．左族精氨酸（Ｌ－Ａｒｓｉｎｉｎｅ）２０００μｍｏｌ／Ｌ可部分对抗ＮＬＡ抑制缺氧加强氯化钾的收缩反应，并完全逆转ＮＬＡ加强氯化钾的收缩反应．硝普钠（ＳｏｄｉｕｍＮｉｔｒｏｐｒｕｓｓｉｄｅ，ＳＮＰ）０．１，１和１０μｍｏｌ／Ｌ可浓度依赖性地抑制缺氧加强氯化钾收缩反应和氯化钾收缩离休猪冠状动脉的作用。

Nitro-L-Arginine (NLA) 200 μmol/L almost abolished the hypoxiapotentiated KCI(20 mmol/L)induced contraction of the porcine isolated coronary artery.and moderately augmented the KCl induced contractile response. L-Arginine(L-Arg)2000 μmol/L partialy reversed the inhibition of NLA on hypoxia-potentiated KCl contractileand completely reversed the augmentation of NLA on the KCl contractile response. SondiumNitroprusside (SNP) 0. 1, 1,10 μmol/L pruduced a contraction-dependent inhibition of thehypoxia-potentiated KCl or KCl-induced cotractile response.