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目的:探讨房颤时心房肌细胞膜上L型Ca2+通道与肌浆网之间的Ca2+信号转导。方法:杂种犬10 条,随机分为正常对照组和单纯房颤组。房颤组用起搏器行右心房快速起搏(500±20)次／分,术后观测24周。正常 对照组不植入起搏器。胶原酶Ⅱ型分离心房肌细胞,用激光共聚焦显微镜检测L型Ca2+通道对细胞内Ca2+浓度变 化的影响;L型Ca2+通道与肌浆网三磷酸肌醇受体(IP3R)和兰尼碱受体(RyR)之间的Ca2+信号转导。结果:(1)L型 Ca2+通道与肌浆网IP3R之间的Ca2+信号转导:正常对照组、单纯房颤组的心房肌细胞在用mibefradil和丁卡因分别 阻滞T型Ca2+通道和RvR后给予细胞膜激动剂时,细胞内Ca2+浓度均升高(分别为1．4000±0．0776和1．5169± 0．4414),组间比较无显著差异(P>0．05);(2)L型Ca2+通道与肌浆网RyR之间的Ca2+信号转导:正常对照组的心房 肌细胞在用mibefradil和肝索分别阻滞T型Ca2+通道和IP3R后给予细胞膜激动剂时,细胞内Ca2+浓度升高(1．5576± 0．1989),单纯房颤组的细胞内Ca2+浓度也升高(1．5372±0．2952),两组间比较元显著差异(P>0．05)。结论:房颤时 L型Ca2+通道与RyR和IP3R之间可能存在信号转导,但其可能在房颤时的细胞内Ca2+超载及异常Ca2+信号转导方 面不起重要作用。
Objective: To investigate the Ca2 + signal transduction between L-type Ca2 + channels and sarcoplasmic reticulum on atrial myocyte membrane during atrial fibrillation. Methods: 10 hybrid dogs were randomly divided into normal control group and simple AF group. Atrial fibrillation group pacemaker right atrial pacing (500 ± 20) times / min, postoperative observation of 24 weeks. Normal control group did not implanted pacemaker. Collagenase Ⅱ was used to separate atrial myocytes and the effect of L-type Ca2 + channel on intracellular Ca2 + concentration was detected by laser scanning confocal microscopy. L-type Ca2 + channels and sarcoplasmic reticulum inositol 1,4,5triphosphate receptor (IP3R) (RyR) between the Ca2 + signal transduction. Results: (1) Ca2 + signal transduction between L-type Ca2 + channels and sarcoplasmic reticulum IP3R: Atrial myocytes in normal control group and atrial fibrillation group were blocked by mibefradil and tetracaine, respectively. Tregs and RvR After intracellular Ca2 + administration, cell Ca2 + concentrations were increased (1.4000 ± 0.0776 and 1.5169 ± 0.4414, respectively), with no significant difference between the two groups (P> 0.05); (2 ) Ca2 + signal transduction between L-type Ca2 + channels and sarcoplasmic reticulum RyR: Atrial myocytes in the normal control group, when given cell membrane agonist after blockade of T-type Ca2 + channel and IP3R respectively by mibefradil and hepatic cord, (1.5576 ± 0.1989). The concentration of intracellular Ca2 + in the atrial fibrillation group also increased (1.5372 ± 0.2952), with a significant difference between the two groups (P> 0.05). CONCLUSIONS: There may be signal transduction between L-type Ca2 + channels and RyR and IP3R during atrial fibrillation, but this may not play an important role in intracellular Ca2 + overload and abnormal Ca2 + signal transduction during atrial fibrillation.