败血症休克过程中心肌肌浆网钙摄取功能的变化及其机理探讨

本工作在大鼠盲肠结扎加穿孔（ＣＬＰ）腹膜炎败血症休克模型上休克不同阶段心肌肌浆网（ＳＲ）钙摄取功能的变化，并探讨了其变化机制。结果显示：败血症休克早期，心肌ＳＲ摄钙初速率降低，但ＳＲ最大摄钙量及Ｃａ＾２＋－ＡＴＰａｓｅ活性没有明显变化；败血症休克晚期，心肌ＳＲ摄钙初速率、最大摄钙量以及Ｃａ＾２＋－ＡＴＰａｓｅ活性显著降低。测定Ｘａ＾２＋，Ｍｇ＾２＋和ＡＴＰ对早、晚期要克大鼠心肌ＳＲ钙泵的亲和力以及

IMPAIRED CALCIUM UPTAKE BY CARDIAC SARCOPLASMIC RETICULUM AND ITS UNDERLVING MECHANISM DURING RAT SEPTIC SHOCK

The underlying mechanism of Ca2 uptake function of cardiac sarcoplasmic reticulum (SR) was investigsted in the rat septic shock model produced by cecal ligstion and puncture (CLP). The results are as follows. During the early phase of sepsis, the initial rate of ATP-dependent Ca2 uptake by SR was decreased, while both the capacity of Ca2 uptake and the activity of Ca2 -ATPase were unaffected. In the late sepsis, the impairment in SR function was even greater as the initial rate and the capacity of Ca2 uptake by SR were significantly decreased, and this was paralleled by a reduction in Ca2 -ATPase activity. Although Ca2 affinity (Km value) to calcium pump and the A0. 5 values for Mg2 and ATP activation on the Ca2 uptake rate were unchanged, during sepsis the phosphorylation of SR vesicles by adding of catalytic subunit of the cAMP-depentent protein kinase (PKA), calmodulin, or the fragment of PKC into Ca2 uptake buffer, failed to stimulate Ca2 uptake activities of SR isolated from early or late septic rats. These data suggest that depression of cardiac SR function is asoavated as sepsis develops, the impairment of SR Ca2 uptake is possibly based on a mechanism of defective phosphorylation of SR rather than the ionic and energic regulatory actions of Ca2 , Mg2 , ATP on cardiac SR.