Protein kinase C is involved in cardioprotective effects of ischemic preconditioning on infarct size and ventricular arrhythmia in rats in vivo
Protein kinase C is involved in cardioprotective effects of ischemic preconditioning on infarct size and ventricular arrhythmia in rats in vivo
复制标题
蛋白激酶C参与缺血预适应对大鼠体内梗死面积和室性心律失常的心脏保护作用
DOI：
--
复制
发表时间：
2000
影响因子：
4.3
通讯作者：
K. Tamura
中科院分区：
文献类型：
--
作者：
Kuniyoshi Matsumura;S. Komori;M. Takusagawa;M. Osada;F. Tanabe;Masahiko Ito;K. Tamura
已知蛋白激酶 C (PKC) 在缺血预适应 (IP) 中发挥重要作用。本研究旨在通过大鼠模型研究 PKC 易位是否与体内 IP 对梗死面积和室性心律失常的心脏保护作用相关。使用麻醉大鼠，测量冠状动脉闭塞 45 分钟期间的心率、收缩压、梗死面积和室性心律失常。检测细胞质和细胞膜部分中的 PKC 活性。使用短暂的 3 分钟缺血期和随后 10 分钟的再灌注来预处理心肌。 Calphostin C 用于抑制 PKC。IP 后梗塞面积显着减小（68.1 (2.5)%，平均值 (S.E.) vs. 45.2 (3.4)%，p < 0.01）。通过使用 Calphostin C 进行预处理，可以消除 IP 带来的梗死面积减少。冠状动脉闭塞 45 分钟期间，IP 减少了室性早搏 (VPC) 总数（1474 (169) 次/45 分钟 vs. 256 (82) 次/45 分钟，p < 0.05）。在短暂缺血发作之前给予 Calphostin C 可以消除由 IP 引起的 VPC 总数的减少。室性心动过速的持续时间和心室颤动的发生率也观察到相同的趋势。细胞膜组分中的 PKC 活性在 IP 后立即短暂增加（100 vs. 142%，p < 0.01），并在 IP 后 15 分钟恢复到基线。 Calphostin C预处理可阻止PKC的易位。PKC的易位在IP对麻醉大鼠梗死面积和室性心律失常的心脏保护作用中发挥重要作用。
Protein kinase C (PKC) has been known to play an important role in ischemic preconditioning (IP). This study was designed to examine whether the translocation of PKC is associated with the cardioprotective effects of IP in vivo on infarct size and ventricular arrhythmias in a rat model.Using anesthetized rats, heart rate, systolic blood pressure, infarct size and ventricular arrhythmias during 45 min of coronary occlusion were measured. PKC activity was assayed in both the cytosolic and cell membrane fraction . Brief 3-min periods of ischemia followed by 10 min of reperfusion were used to precondition the myocardium. Calphostin C was used to inhibit PKC.Infarct size was significantly reduced by IP (68.1 (2.5)%, mean (S.E.) vs. 45.2 (3.4)%, p < 0.01). The reduction in infarct size by IP was abolished by pretreatment with calphostin C. The total number of ventricular premature complex (VPC) during 45 min of coronary occlusion was reduced by IP (1474 (169) beats/45 min vs. 256 (82) beats/45 min, p < 0.05). The reduction the total number of VPC induced by IP was abolished by the administration of calphostin C before the episode of brief ischemia. The same tendency was observed in the duration of ventricular tachycardia and the incidence of ventricular fibrillation. PKC activity in the cell membrane fraction transiently increased immediately after IP (100 vs. 142%, p < 0.01) and returned to baseline 15 min after IP. Pretreatment with calphostin C prevented the translocation of PKC.The translocation of PKC plays an important role in the cardioprotective effect of IP on infarct size and ventricular arrhythmias in anesthetized rats.