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本研究证明，脓毒症（结扎盲肠及穿刺，ＣＰＬ）大鼠心肌肌膜腺苷酸环化酶（ＡＣ）的活性及其部分纯化的ＡＣ最大活性，在早期脓毒症（ＥＳ，ＣＬＰ后９ｈ）时明显增高，在晚期脓毒症（ＬＳ，ＣＬＰ后１８ｈ）时明显降低。其心肌肌膜蛋白激酶Ｃ（ＰＫＣ）的活性亦呈现类似变化。ＥＳ和ＬＳ大鼠心肌肌膜ＡＣ的增敏和失敏与ＰＫＣ的激活和抑制有关。上述ＡＣ和ＰＫＣ的双相变化不是肾上腺能β－受体和α１－受体系统依赖的。ＥＳ大鼠心肌肌膜ＰＫＣ的激活和ＡＣ的增敏与Ｍ－胆碱受体系统有关；而ＬＳ大鼠心肌肌膜ＰＫＣ的抑制和ＡＣ的失敏与Ｍ－胆碱受体系统无关。
This study demonstrated that the activity of myocardial myocyte adenylate cyclase (AC) and the fractional AC maximal activity of sepsis (ligature cecal and puncture, CPL) in rats were significantly decreased in early sepsis (ES, CLP 9h) was significantly higher in advanced sepsis (LS, 18h after CLP) was significantly reduced. Its cardiac muscle protein kinase C (PKC) activity also showed a similar change. Sensitization and desensitization of AC in sarcolemma of ES and LS rats are related to the activation and inhibition of PKC. The biphasic changes of AC and PKC above are not dependent on the adrenergic beta -receptor and alpha1-receptor systems. Activation of PKC and AC sensitization in ES rat myocardium are related to the M-cholinergic receptor system; whereas inhibition of PKC and AC desensitization in LS rat myocardium are independent of M-cholinergic receptor system.