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目的：研究钙增敏剂ＭＣＩ－１５４ 对内毒素休克大鼠心肌钙稳态的影响。方法：甲腈吡酮或ＭＣＩ－１５４ 治疗内毒素休克大鼠后１、３、５ ｈ，分别测定心肌组织、线粒体、肌浆网（ＳＲ）的钙含量；离体分离内毒素休克大鼠心肌细胞，分别与１×１０－ ３、１×１０－ ２、１×１０－ １ｍ ｍ ｏｌ／Ｌ甲腈吡酮或ＭＣＩ－１５４孵育，利用Ｆｕｒａ ２－ＡＭ 测定心肌细胞胞浆钙浓度（［Ｃａ２＋ ］ｉ）。结果：内毒素休克后，心肌组织、线粒体、ＳＲ钙含量明显增加。甲腈吡酮治疗后，上述指标进一步升高；而ＭＣＩ－１５４ 治疗后，心肌组织、线粒体、ＳＲ钙含量无明显增加，治疗后３、５ ｈ 值同单纯生理盐水（ＮＳ）治疗组无明显差别，显著低于甲腈吡酮治疗组值。内毒素休克大鼠心肌细胞［Ｃａ２＋ ］ｉ明显高于对照组，甲腈吡酮与内毒素休克心肌细胞孵育后，［Ｃａ２＋ ］ｉ随药物浓度增大而显著升高；不同浓度的ＭＣＩ－１５４均不明显升高心肌细胞［Ｃａ２＋ ］ｉ。结论：ＭＣＩ－１５４用于内毒素休克治疗时，不进一步加重心肌钙稳态失衡及心肌细胞内钙超载。
Objective: To study the effect of calcium sensitizer MCI-154 on calcium homeostasis in endotoxic shock rats. Methods: The contents of calcium in myocardial tissue, mitochondria and sarcoplasmic reticulum (SR) were measured at 1 h, 3 h and 5 h after treatment with either acetonitril or MCI-154. Endotoxic shock Cells were incubated with 1 × 10-3, 1 × 10-2, 1 × 10-1 m mol / L MCI-154, and the cytosolic calcium concentration ([Ca2 + ] I). Results: After endotoxin shock, the content of SR in myocardial tissue, mitochondria and SR increased obviously. After MCI-154 treatment, the above parameters were further increased. After MCI-154 treatment, there was no significant increase in myocardial calcium, calcium content in myocardium, mitochondria and mitochondria, while the values at 3,5 h after treatment were not significantly different from those in NS group The difference was significantly lower than the nitrile-treated group values. The [Ca2 +] i in endotoxic shock rats was significantly higher than that in control group. [Ca2 +] i increased with the increase of drug concentration after the incubation with tetraglitazone and endotoxic shock cardiomyocytes. Different concentrations of MCI-154 No significant increase in myocardial cells [Ca2 +] i. Conclusion: MCI-154 is not used to increase the imbalance of calcium homeostasis and intracellular calcium overload in endotoxic shock.