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应用ＡＲ－ＣＭ－ＭＩＣ阳离子测定系统，研究ＴＭＢ－８对体外新生ＳＤ大鼠单个脑细胞内游离钙的抑制作用及其机制。结果表明，在无细胞外钙情况下，静息［Ｃａ２＋］ｉ为７９±１３ｎｍｏｌ·Ｌ－１。ＴＭＢ－８１０，３０μｍｏｌ·Ｌ－１能明显降低静息［Ｃａ２＋］ｉ。ＴＭＢ－８１００μｍｏｌ·Ｌ－１对高钾去极化引起的［Ｃａ２＋］ｉ显著增高无明显影响。在细胞外钙为１．３ｍｍｏｌ·Ｌ－１时，去甲肾上腺素诱导的细胞内［Ｃａ２＋］ｉ升高可部分被ＴＭＢ－８抑制；ＴＭＢ－８（３０μｍｏｌ·Ｌ－１）对ＢＨＱ引起的［Ｃａ２＋］ｉ的升高无明显抑制作用。而当细胞外液［Ｃａ２＋］ｉ为０时，ＴＭＢ－８几乎完全抑制了去甲肾上腺素和ＢＨＱ的作用。提示ＴＭＢ－８降低脑细胞内游离钙的作用机制是通过促使细胞内钙进入肌浆网以抑制内钙的释放，并通过饱和肌浆网内Ｃａ２＋间接地阻滞细胞膜钙通道
AR-CM-MIC cationic assay system was used to study the inhibitory effect of TMB-8 on intracellular free calcium in neonatal SD rats and its mechanism. The results showed that the resting [Ca2 +] i was 79 ± 13 nmol·L-1 in the absence of extracellular calcium. TMB-810, 30μmol·L-1 can significantly reduce resting [Ca2 +] i. TMB-8100μmol·L-1 had no significant effect on the significant increase of [Ca2 +] i induced by high potassium depolarization. The increase of [Ca2 +] i in noradrenaline-induced intracellular calcium was partially inhibited by TMB-8 when the extracellular calcium was 1.3 mmol·L-1; the effect of TMB-8 (30 μmol·L-1) No significant inhibition of [Ca2 +] i increase. TMB-8 almost completely inhibited the effect of norepinephrine and BHQ when [Ca2 +] i was 0 in extracellular fluid. Tip TMB-8 to reduce intracellular free calcium mechanism of action is through the intracellular calcium into the sarcoplasmic reticulum to inhibit the release of calcium and saturating the sarcoplasmic reticulum Ca2 + indirectly through the cell membrane calcium channel