摘要
目的 由吡那地尔诱导犬右心室肌细胞产生“全或无”复极,观察奎尼丁对这种跨壁复极离散的影响。方法 应用标准玻璃微电极技术在1000ms刺激周长下,记录犬右心室肌细胞不同部位(外膜下、M区、内膜下)在不同情况[正常对照、吡那地尔(2 5μmol/L)、吡那地尔( 2 5μmol/L) +奎尼丁(5μmol/L) ]的动作电位。结果 吡那地尔( 2 5μmol/L)在3层细胞产生“全或无”复极,使跨壁复极离散增大,动作电位时程跨壁复极离散由(48 .5±9 .2)ms升为(128. 7±13. 5)ms(P<0. 01),进一步灌注奎尼丁(5μmol/L)后,减为(54 .3±10 .8)ms(P<0. 01)。奎尼丁部分恢复动作电位2相平台,延长了被吡那地尔缩短的动作电位时程。结论 在犬右心室肌组织,奎尼丁(5μmol/L)减小了由吡那地尔造成的跨壁复极离散,维持了跨壁电稳定性。
Objective On the basis that pinacidil can produce an “all or none” repolarization in right ventricular wall of canine, to observe the effects of quinidine on the marked transmural dispersion of repolarization. Recent studies have shown that ventricular myocardium is composed of at least 3 electrophysiological distinct cell types: epicardial, endocardial, and midcardial cells. Differences in the response of the 3 cell types to pharmacologic agents and/or pathophysiological states often result in amplification of intrinsic electrical heterogeneities, thus providing a substrate as well as a trigger for the development of arrhythmias. The study was designed to observe the right ventricular transmural heterogeneity in vitro canine heart tissue preparation level.Methods The strips were isolated from the anterior wall of the right ventricular of canine. The preparations perfused with oxygenated (95%O 2 /5% CO 2) Tyrode′s solution. The tissues were stimulated at basic cycle lengths of 1000 ms. Standard microelectrode techniques were used. Transmembrane action potentials were recorded from epicardial, midcardial and endocardial cells respectively from right ventricular free wall of canine on different conditions [perusing with Tyrode′s solution (Control), pinacidil (2.5 μmol/L), and quinidine (5 μmol/L) in turn]. Results Compared with that of endocardial cells, the action potentials of canine ventricular epicardial and midcardial cells had more obvious spike and dome morphology. Pinacidil (2.5 μmol/L) caused a loss of the dome of transmembrane action potentials and a marked abbreviation of the action potential duration(APD) in right ventricular epicardial and midcardial cells, especially in epicardial cells,but not in endocardial cells (n=10). With pinacidil (2.5 μmol/L), in epicardial cells, phase 2 amplitude of action potentials decreased from (117.7±9.3) mV to (71.3±6.4) mV (P<0.01), and 90% of the APD 90 decreased from (198.2±20.8) ms to (103.9±13.5) ms (P<0.01). The transmural dispersion of action potential duration increased from (48.5±9.2) ms to (128.7±13.5) ms (P<0.01). Quinidine (5 μmol/L) effectively prolonged the APD abbreviated by pinacidil, restored or partly restored the dome of transmembrane action potentials of epicardial and midcardial cells but not of endocardial cells (n=10). In epicardial cells phase 2 amplitude increased from (71.3±6.4) mV to (106.6±7.7) mV (P<0.01), and 90% of the APD 90 increased from (103.9±13.5) ms to (185.9±15.7) ms (P<0.01). The transmural dispersion of action potential duration significantly decreased from (128.7±13.5) ms to (54.3±10.8) ms (P<0.01). Quinidine reduced pinacidil-induced transmural dispersion of phase 2 amplitude and the APD in right ventricular wall of canine. Conclusion By restoring the dome and the APD of the epicardial and midcardial cells action potentials, quinidine (5 μmol/L) could reduce the marked transmural dispersion of repolarization caused by pinacidil.
出处
《中华心血管病杂志》
CAS
CSCD
北大核心
2005年第4期369-371,共3页
Chinese Journal of Cardiology
