摘要
目的 研究莫索尼定 (Mox)对窦房结起搏细胞是否具有电生理作用及其相关受体以探讨Mox治疗实验性心律不齐的机理。方法 利用细胞内微电极技术记录窦房结细胞AP。结果 Mox(0 .3～ 3mmol·L- 1)浓度依赖性地降低AP的舒张期除极速率 (VDD) ,减慢自发搏动速率 (RPF) ,延长AP复极达 5 0 %及 90 %的时程 (APD50 和APD90 )。 1和 3mmol·L- 1Mox还明显增大最大舒张电位 (MDP)的绝对值。预先灌流α2 受体拮抗剂育亨宾 (1.0 μmol·L- 1,2 0min)取消Mox降低VDD ,延长APD50 和APD90 的作用 ;拮抗较低浓度Mox降低RPF和增大MDP的作用。育亨宾处理标本后 ,Mox显著增加AP幅度和最大除极速率。结论 Mox延长兔窦房结起搏细胞动作电位APD50 和APD90 以及降低VDD的作用主要由α2 受体中介。Mox增大MDP绝对值和减慢RPF的作用则与α2
AIM To explain the mechanism of moxonidine(Mox) in treatment of experimental arrhythmia by studying whether Mox has the electrophysiologic effects on sinoatrial node(SAN) pacemaker cells and which are its related receptors. METHODS Intracellular microelectrode technique was used to record action potentials(AP) in the rabbit SAN pacemaker cells. RESULTS Mox (0.3-3.0 mmol·L -1) concentration-dependently decreased the velocity of diastolic (phase 4) depolarization (VDD) and rate of pacemaker firing (RPF),and prolonged the duration at 50% and 90% repolarization (APD 50 and APD 90) of AP in the rabbit SAN pacemaker cells. Mox at 1.0 and 3.0 mmol·L -1 significantly increased maximal diastolic potential (MDP). The effects of Mox on VDD, APD 50 and APD 90 were inhibited completely by yohimbine (1.0 μmol·L -1 pre-perfused for 20 min), while those on RPF and MDP were inhibited by yohimbine at lower concentration of Mox. Moreover, in the preparations pre-treated with yohimbine, Mox increased AP amplitude and maximal depolarization rate of phase 0 ( max) significantly. CONCLUSION Mox prolongs the APD 50 and APD 90, and decreases the VDD in the rabbit SAN pacemaker cells, which are mainly mediated by α 2-adrenoceptors. In addition, the effects of Mox on MDP and RPF are partially mediated by α 2-adrenoceptors.
出处
《中国药理学与毒理学杂志》
CAS
CSCD
北大核心
2002年第4期250-254,共5页
Chinese Journal of Pharmacology and Toxicology
基金
河北省自然科学基金 (30 2 481)
河北省科学技术研究与发展计划项目基金 (0 2 2 76 10 4D 2 6 )~~
