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本实验在结扎大鼠盲肠并穿孔（ＧＬＰ）所复制的败血症休克模型上观察了早、晚期败血症休克时大鼠心肌Ｍ受体结构和功能的变化。结果发现：早期休克时Ｍ受体在质膜的分布增加，在轻囊的分布减少，表现为质膜３Ｈ－ＱＮＢ最大结合量（Ｂｍａｘ）增加３３．７３％；轻囊Ｂｍａｘ降低２６．９０％；晚朝体克时Ｍ受体在经囊的分布增加，在质膜的分布减少（质膜Ｂｍａｘ值降低３９．２５％，轻囊Ｂｍａｘ值增加２９．２１％）。同时心肌Ｍ受体蛋白磷酸化程度也出现早期降低和晚期增加的双相变化。推测休克时心肌Ｍ受体的改变可能与休克时心肌功能障碍有关。
In this study, we observed the changes of myocardial M receptor structure and function in rats with early and late septic shock under the model of sepsis shocked by ligating rat cecal perforation (GLP). The results showed that the distribution of M receptor in the plasma membrane increased and the distribution of the M capsule decreased in the early shock, showing a 33.73% increase in the maximum plasma membrane bound 3H-QNB (Bmax) and a decrease of 26.90% ; In late gynoecium, the distribution of M receptor increased in the capsule and decreased in the plasma membrane (the plasma membrane Bmax decreased by 39.25% and the light capsule Bmax increased by 29.21%). At the same time, myocardial M receptor protein phosphorylation also showed an early decrease and late increase biphasic changes. It is speculated that the change of myocardium M receptor during shock may be related to myocardial dysfunction during shock.