卡托普利对缺氧复氧乳鼠心室肌细胞游离钙和钠钙交换电流的影响

 目的观察卡托普利预处理对缺氧复氧乳鼠心室肌细胞游离钙和钠钙交换电流(Na⁺/Ca²⁺exchange current,I_Na-Ca)的影响。方法建立培养乳鼠心肌细胞缺氧/复氧损伤模型。Flou-3/AM负载染色,应用流式细胞分析技术,测定细胞内钙离子浓度(Ca²⁺]_i);利用全细胞膜片钳技术,观察I_Na-Ca的变化。结果与正常对照组比较,缺氧复氧可显著增加Ca²⁺]_i和I_Na-Ca。与缺氧复氧组比较,卡托普利呈浓度依赖性抑制缺氧复氧时Ca²⁺]_i增加,减少I_Na-Ca的增加。但Ca²⁺]_i和I_Na-Ca仍高于正常对照组。结论心肌细胞缺氧复氧可引起Ca²⁺]_i的异常升高,与I_Na-Ca的异常增加有关;卡托普利预处理可能通过轻度增加I_Na-Ca及其Ca²⁺]_i而触发心脏延迟保护作用,抑制后续缺氧复氧引起的I_Na-Ca及其Ca²⁺]_i的异常增加。

Influence of Captopril on Intracellular Calcium Concentration and Na+/Ca2+ Exchange Current in Cardiac My ocytes of Neonatal Rat Undergone Anoxia-Reoxygenation Injury

OBJECTIVE To observe the influence of captopril on in tracellular free calcium concentration(Ca²⁺]_i) and Na⁺/Ca²⁺ exchange current in the cardiac myocytes of the neonatal rat undergone anoxia-reoxygenation injury.METHODS The anoxia-reoxygenation models were developed.The cultured ventricular myocytes of neonatal rat were established and divided into normal,anoxia-reoxygenation and captopril preconditioning groups.By using Flou-3/AM loading and flow cytometry technique,the Ca²⁺]_i was observed,and whole-cell patch clamp technique was used to record the Na⁺/Ca²⁺exchange current.RESULTS ①Compared with normal group,Ca²⁺]_i and Na⁺/Ca²⁺ exchange current in anoxia-reoxygenation group were increased significantly(P<0.01).②Compared with anoxia-reoxygenation group,the captopril precondition group resulted in a significant decrease of Ca²⁺]_i in a concentration dependent manner,and Na⁺/Ca²⁺ exchange current was also decreased.③Compared with normal oxygen condition,the captopril precondition group resulted in a light increase of Ca²⁺]_i and Na⁺/Ca²⁺ exchange current.CONCLUSION The anoxia-reoxygenation injury in cardiac myocytes resulted in an abnormal increase of Ca²⁺]_i by increasing Na⁺/Ca²⁺ exchange current.Late preconditioning in cardiac myocytes is triggered by captopril which slightly increased Na⁺/Ca²⁺ exchange current and Ca²⁺]_i,and restrained the abnormal increasing of Na⁺/Ca²⁺ exchange current and calcium overload induced by subsequenced anoxia-reoxygenation injury.