摘要
丁基苯酞（ＮＢＰ）对脑缺血损伤有保护作用，为探讨其作用机制，采用离体大鼠尾动脉环为标本，观察了ＮＢＰ对ＫＣｌ和去甲肾上腺素所致尾动脉收缩的影响，以及ＮＢＰ与细胞内，外钙的关系．结果表明：ＮＢＰ在大剂量时，能非竞争性及竞争性地抑制ＫＣｌ及去甲肾上腺素引起的血管收缩．ｐＤ＇２及ｐＡ２值分别为３．５７±０．１４及４．８６±０．１３，表明作用较弱．ＮＢＰ１００μｍｏｌ·Ｌ－１对去甲肾上腺素的内源性钙收缩有抑制作用，而对外源性钙收缩无影响．
Previous studies had shown that dl-3-n -butylphthalide (NBP) could protect rat from cerebral ischemic damage subjected to middle cerebral artery occlusion. In order to clarify the mechanism of pharmacological action of NBP, the effects of NBP on contraction of rat isolated tail artery induced by KCl or norepinephrine (NE) were studied. The results show that NBP at the concentration of 100 or 500 μmol·L -1 competitively inhibited the contraction induced by NE and non-competitively inhibited the contractioninduced by KCl. The values of pA 2 and pD 2 'were 4.86 ±0.13 and 3.57±0.14 respectively. Compared with nimodipine (pD 2 '=8.50±0.20), NBP had weaker influence on voltage-dependent calcium channel. It is also shown that NBP at concentration of 100 μmol·L -1 inhibited the contraction induced by NE-dependent intracellular calcium, but NBP had no effect on contraction induced by extracellular calcium. The results suggest that the inhibiting action of NBP on intracellular calcium release initiated by NE in vascular smooth muscle may be responsible for the protective effect of NBP on brain ischemic damage.
出处
《中国药理学与毒理学杂志》
CSCD
北大核心
1996年第2期113-115,共3页
Chinese Journal of Pharmacology and Toxicology
