败血症大鼠心肌钙通道分布的变化

CHANGES IN THE CALCIUM CHANNELS IN RAT CARDIAC CELLS DURING SEPSIS

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。

Changes in the number of calcium channels in two, subcellular fractions, the sarcolemma and the light vesicle, of rat cardic cells were studied during sepsis. Sepsis was induced by cecal ligation and puncture (CLP). The results showed that some of the calcium channels in the light vesicle translocated to the sarcolemma during the early sepsis (9 h after CLP) while during the late sepsis (18 h after CLP). Some of these in the sarcolemma translocated to the light vesicle. The mechanisms of redistribution of the calcium channels in the sarcolemma and the light vesicle during sepsis was not associated to the phosphorylation of the calcium channels by cAMP dependent protein kinase (PKA),Ca(2+)/calmodulin dependent protein kinase (PKM) and protein kinase C (PKC). Since β-adrenrgic recptors, muscarinic cholinergic receptors and Na+/K+-ATPase were also redistributed during sepsis, it is suggested that the redistribution might be non-specific.