Levites R, Bodenheimer M M, Helfant R H
Circulation. 1975 Dec;52(6):1050-5. doi: 10.1161/01.cir.52.6.1050.
Previous studies have shown that nitroglycerin (TNG) exerts beneficial electrophysiological effects in the setting of acute myocardial ischemia. To investigate the basis for these actions, the effects of TNG during coronary occlusion were studied in 19 anesthetized mongrel dogs. Refractory periods (obtained by extrastimulus method) and conduction times measured from local electrograms were determined in potentially ischemic and nonischemic areas prior to and after varying periods of occlusion of the left anterior descending coronary artery and following administration of TNG (300-400 mug intravenous bolus followed by an infusion titrated to reduce systolic blood pressure by 20 mm Hg). Following 15 minutes of occlusion, refractory periods in the ischemic zones shortened to 83% of control (P less than 0.001) resulting in a difference between refractory periods in the nonischemic and ischemic zones of 17.7%. After TNG administration this difference was decreased to 10.0% (P less than 0.001). However, with periods of occlusion of 60-90 min TNG did not significantly affect the difference of refractory periods. TNG had no significant effects on conduction times in nonischemic or ischemic areas. In six dogs, the effects of coronary occlusion and TNG on ventricular automaticity were examined by induction of complete heart block. The idioventricular rate and ventricular escape intervals after cessation of ventricular overdrive were used as indices of automaticity. Control idioventricular rates (62.5 +/- 3.7 beats/min) remained unchanged following both coronary occlusion (62.0 +/- 3.9) and TNG administration (60.7 +/- 3.2). Similarly, mean control escape intervals (1.84 +/- 0.2 sec) did not change after occlusion (1.78 +/- 0.3 sec) or TNG administration (1.86 +/- 0.2 sec). In conclusion, these observations suggest that 1) TNG enhances the electrical stability of the acutely ischemic myocardium by decreasing the difference of refractory periods between nonischemic and ischemic areas in the immediate period following occlusion, 2) since TNG has no significant effects on ventricular automaticity, its beneficial effects might be limited in suppression of arrhythmias of re-entrant origin.
先前的研究表明,硝酸甘油(TNG)在急性心肌缺血情况下发挥有益的电生理作用。为了探究这些作用的基础,在19只麻醉的杂种犬中研究了冠状动脉闭塞期间TNG的作用。在左前降支冠状动脉闭塞不同时间段之前和之后,以及给予TNG(静脉推注300 - 400微克,随后进行输注,调整剂量以使收缩压降低20毫米汞柱)之后,通过额外刺激法获得的不应期以及从局部心电图测量的传导时间,在潜在缺血和非缺血区域进行测定。闭塞15分钟后,缺血区的不应期缩短至对照的83%(P小于0.001),导致非缺血区和缺血区不应期之间的差异为17.7%。给予TNG后,这种差异降至10.0%(P小于0.001)。然而,在闭塞60 - 90分钟时,TNG对不应期差异没有显著影响。TNG对非缺血或缺血区域的传导时间没有显著影响。在6只犬中,通过诱导完全性心脏传导阻滞来研究冠状动脉闭塞和TNG对心室自律性的影响。心室超速驱动停止后的心室自主心律和心室逸搏间期用作自律性指标。冠状动脉闭塞(62.0±3.9次/分钟)和给予TNG(60.7±3.2次/分钟)后,对照心室自主心律(62.5±3.7次/分钟)均保持不变。同样,平均对照逸搏间期(1.84±0.2秒)在闭塞后(1.78±0.3秒)或给予TNG后(1.86±0.2秒)没有变化。总之,这些观察结果表明:1)TNG通过在闭塞后的即刻减少非缺血区和缺血区之间的不应期差异来增强急性缺血心肌的电稳定性;2)由于TNG对心室自律性没有显著影响,其有益作用在抑制折返性心律失常方面可能有限。