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本研究用结扎盲肠及穿刺（ＣＬＰ）引起败血症。结果证明：大鼠心肌钙通道在早期败血症（ＥＳ，ＣＬＰ后９ｈ）时由心肌轻型囊泡向心肌肌膜转运增多；在晚期败血症（ＬＳ，ＣＬＰ后１８ｈ）时由心肌肌膜向心肌轻型囊泡转运增多。败血症时大鼠心肌肌膜和心肌轻型囊泡钙通道的再分布与ｃＡＭＰ依赖性蛋白激酶（ＰＫＡ），Ｃａ（２＋）／钙调素依赖性蛋白激酶（ＰＫＭ）和蛋白激酶Ｃ（ＰＫＣ）磷酸化作用无关。败血症时大鼠心肌肌膜和心肌轻型囊泡上肾上腺能β－受体、Ｍ－胆碱受体和Ｎａ＋／Ｋ＋ＡＴＰａｓｅ的变化规律和钙通道的一样，它们可能是败血症时的一种非特异性变化。
In this study, septicemia was induced by ligature cecal and puncture (CLP). The results demonstrated that calcium channels in rat myocardium increased from light myocardium to myocardial sarcolemmal in early septicemia (ES, 9h after CLP). In late septicemia (18h after CLP, CLP) Bubble transport increased. The redistribution of calcium channels in the myocardium and myocardium of rats with sepsis was associated with cAMP-dependent protein kinase (PKA), Ca (2 +) / calmodulin-dependent protein kinase (PKM) and protein kinase C (PKC) Has nothing to do with the role. The changes of adrenal β -receptor, M-cholinergic receptor and Na + / K + ATPase in rat myocardium and myocardial light vesicles in sepsis are the same as those in calcium channel, which may be a nonspecific change in sepsis .