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用荧光分光光度法及同位素放射免疫分析法检测丙泊酚（３０－３００μｍｏｌ·Ｌ－１）影响大鼠肺动脉平滑肌细胞（ＰＡＳＭＣ）内游离钙离子浓度（［Ｃａ２＋］ｉ）与肌醇－１，４，５－三磷酸（ＩＰ３）合成作用，以探讨丙泊酚舒张肺动脉平滑肌的作用机理．结果表明，与丙泊酚共同培养７２ｈ，对ＰＡＳＭＣ［Ｃａ２＋］ｉ基础水平无明显影响，但可浓度依赖性抑制去甲肾上腺素（ＮＥ３μｍｏｌ·Ｌ－１）引起的［Ｃａ２＋］ｉ升高作用；当细胞外液无钙或存在钙通道阻滞剂维拉帕米（３０μｍｏｌ·Ｌ－１）时，丙泊酚抑制ＮＥ升高［Ｃａ２＋］ｉ作用被增强；丙泊酚还可浓度依赖性抑制ＮＥ促进ＩＰ３合成作用．结果提示丙泊酚舒张血管平滑肌作用与抑制ＩＰ３介导的细胞内钙释放密切相关．
Fluorescence spectrophotometry and isotope radioimmunoassay were used to detect the effect of propofol (30-300μmol·L-1) on the intracellular free calcium concentration ([Ca2 +] i) and inositol-1 in rat pulmonary arterial smooth muscle cells (PASMCs) 4,5-triphosphate (IP3) synthesis to explore the mechanism of propofol relaxation of pulmonary artery smooth muscle. The results showed that incubation with propofol for 72h had no significant effect on the basal level of [Ca2 +] i in PASMC but inhibited the elevation of [Ca2 +] i induced by NE3μmol·L-1 in a concentration-dependent manner. Propofol inhibited the elevation of [Ca2 +] i in NE while extracellular calcium was not present or calcium channel blocker verapamil was present (30μmol·L-1). Propofol also inhibited in a concentration-dependent manner NE promotes IP3 synthesis. The results suggest that the effect of propofol on vascular smooth muscle relaxation is closely related to the inhibition of IP3-mediated intracellular calcium release.