Wang Ru-Xing, Li Xiao-Rong, Lai Li-Hong, Wu Xiao-Qing, Chen Yan-Fen, Song Jian-Ping, Yang Xiang-Jun, Jiang Wen-Ping
Department of Cardiology, Affiliated Wuxi People's Hospital of Nanjing Medical University, Wuxi 214023, China.
Zhonghua Xin Xue Guan Bing Za Zhi. 2009 Feb;37(2):108-11.
To investigate the effects of docosahexaenoic acid (DHA) on action potential (AP) and transient outward potassium current (I(to)) on ventricular myocytes of Sprague-Dawley rat.
Calcium-tolerant ventricular myocytes were isolated by enzyme digestion. The changes of AP and I(to) with increasing DHA at concentrations of 0, 10, 20, 40, 60, 80, 100, 120 and 200 micromol/L were recorded by whole-cell patch clamp configuration.
(1) Action potential durations (APDs) were not affected by DHA at concentrations from 0 micromol/L to 30 micromol/L, while APDs were gradually prolonged in proportion with increasing DHA concentrations from 30 micromol/L to 200 micromol/L within 5 minutes and remained stable thereafter. APD(25), APD(50) and APD(75) were (7.7 +/- 2.0) ms, (21.2 +/- 3.5) ms, and (100.1 +/- 9.8) ms respectively at 100 micromol/L DHA. APD(25), APD(50), and APD(75) were (15.2 +/- 4.0) ms, (45.7 +/- 6.8) ms, and (215.6 +/- 15.7) ms respectively at 200 micromol/L DHA. (2) I(to) was gradually reduced with the increasing DHA concentrations from 10 micromol/L to 200 micromol/L. I(to) was blocked by DHA in a dose-dependent manner. I(to) current density was (30.1 +/- 7.2) pA/pF at DHA concentration of 60 micromol/L and its half-inhibition concentration was 58.3 micromol/L.
APDs are gradually prolonged while I(to) reduced with increasing concentrations of DHA which might contribute to the anti-arrhythmia mechanisms of DHA.
研究二十二碳六烯酸(DHA)对Sprague-Dawley大鼠心室肌细胞动作电位(AP)和瞬时外向钾电流(I(to))的影响。
采用酶消化法分离耐钙心室肌细胞。采用全细胞膜片钳记录0、10、20、40、60、80、100、120和200 μmol/L浓度DHA增加时AP和I(to)的变化。
(1)0 μmol/L至30 μmol/L浓度的DHA对动作电位时程(APD)无影响,而在5分钟内,随着DHA浓度从30 μmol/L增加到200 μmol/L,APD逐渐延长,并在此后保持稳定。在100 μmol/L DHA时,APD(25)、APD(50)和APD(75)分别为(7.7±2.0) ms、(21.2±3.5) ms和(100.1±9.8) ms。在200 μmol/L DHA时,APD(25)、APD(50)和APD(75)分别为(15.2±4.0) ms、(45.7±6.8) ms和(215.6±15.7) ms。(2)随着DHA浓度从10 μmol/L增加到200 μmol/L,I(to)逐渐降低。DHA以剂量依赖性方式阻断I(to)。在60 μmol/L DHA浓度下,I(to)电流密度为(30.1±7.2) pA/pF,其半抑制浓度为58.3 μmol/L。
随着DHA浓度增加,APD逐渐延长,而I(to)降低,这可能是DHA抗心律失常机制的原因。