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本文观察了败血症休克时心肌终囊处肌浆网（ＳＲ）钙释放通道Ｒｙａｎｏｄｉｎｅ受体的变化及其膜脂质微环境改变的机制。结果发现，晚期败血症休克大鼠心肌肌浆网（ＣＳＲ）Ｒｙａｎｏｄｉｎｅ与受体结合的Ｂｍａｘ降低４１．３％（Ｐ＜０．０１），Ｋｄ值无明显变化。钙离子可明显激活３Ｈ－Ｒｙａｎｏｄｉｎｅ与其受体的结合，其激活曲线在钙离子浓度为５×１０－５ｍｏｌ／Ｌ时达到饱和状态。咖啡因，ＡＴＰ，ＡＭＰ－ＰＣＰ都可浓度依赖性地促进３Ｈ－Ｒｙａｎｏｕｉｎｅ与受体的结合，而钌红（ＲｅｔｈｅｎｉｕｍＲｅｄ），氯化镁则浓度依赖性地抑制其结合。但败血症休克时上述激动剂或抑制剂的Ａ０．５和ＩＣ５０均无明显改变。用磷脂酶Ａ２消化假手术动物ＳＲ后，其３Ｈ－Ｒｙａｎｏｄｉｎｅ与受体的结合明显降低，将磷脂酰胆碱（ＰＣ），磷脂酰乙醇胺（ＰＥ）和磷脂酰丝氨酸（ＰＳ）分别参入到上述消化后的ＣＳＲ膜中可明显提高３Ｈ－Ｒｙａｎ－ｏｄｉｎｅ与受体的结合。同时，ＰＣ，ＰＥ，ＰＳ分别参入ＣＳＲ中可显著改善败血症休克时ＣＳＲ３Ｈ－Ｒｒａｎ－ｏｄｉｎｅ与受体的低结合状态。上述结果表明，败血症休克时，内毒素抑制大鼠ＣＳＲ３Ｈ－Ｒｙａｎｏｄｉｎｅ受体结合与其过度激活磷?
In this paper, the changes of Ryanodine receptor in the calcium release channel of sarcoplasmic reticulum (SR) and the mechanism of membrane lipid microenvironment change in septic shock were observed. The results showed that the Bmax of Ryanodine binding to the receptor decreased 41.3% (P <0.01), and the Kd value did not change significantly in septic shock rats. The binding of 3H-Ryanodine to its receptor was obviously activated by calcium ion, and its activation curve reached the saturation state when the calcium ion concentration was 5 × 10-5mol / L. Both caffeine, ATP and AMP-PCP promoted the binding of 3H-Ryanouine to the receptor in a concentration-dependent manner, whereas the redness of RetheniumRed and magnesium chloride inhibited the binding in a concentration-dependent manner. However, there was no significant change in A0.5 and IC50 of the above agonists or inhibitors in septic shock. After digestion of SR with phospholipase A2, the binding of 3H-Ryanodine to the receptor was significantly reduced, and phosphatidylcholine (PC), phosphatidylethanolamine (PE) and phosphatidylserine (PS) After the CSR film can significantly improve 3H-Ryan-odine and receptor binding. At the same time, the incorporation of PC, PE and PS into CSR significantly improved the low binding of CSR3H-Rran-odine to the receptor during septic shock. The above results indicate that endotoxin inhibits the binding of CSR3H-Ryanodine receptors to over-activated phosphorus in septic shock in rats