Boudoulas H, Lewis R P, Rittgers S E, Leier C V, Vasko J S
J Cardiovasc Pharmacol. 1979 Sep-Oct;1(5):503-13.
Diastolic time (DT) calculated as the cycle length minus electromechanical systole (QS2) has a nonlinear relationship to heart rate (HR), increasing rapidly as rates fall below 75. The effect of propranolol on DT was studied in 150 patients with coronary artery disease. Patients were divided into three groups. Group I included patients with stable angina pectoris: propranolol (2.5 mg, i.v.) significantly increased DT from 411 +/- 18 to 527 +/- 22 msec (p less than 0.001) in 23 patients of group I; therapy with propranolol (mean daily dose 200 +/- 15 mg) increased DT from 446 +/- 29 to 766 +/- 26 msec (p less than 0.001) in 15 patients with stable angina. Group II was made up of patients with acute myocardial infarction: Propranolol (2.5 mg, i.v.) increased DT from 379 +/- 16 to 458 +/- 24 (p less than 0.001) in 18 of these patients. Group III included patients with recent coronary bypass surgery: propranolol (2.5 mg, i.v.) increased DT from 323 +/- 9 to 468 +/- 24 msec (p less than 0.001) in 14 patients 7 days after surgery. In addition, DT at 15 hr and 2 weeks after surgery was compared in 30 patients maintained on propranolol (mean daily dose, 155 +/- 11 mg preoperative and 68 +/- 9 mg postoperative) and 50 other patients who underwent coronary bypass surgery not on propranolol. DT was greater in propranolol patients (546 +/- 21 vs. 388 +/- 16 msec, p less than 0.001), preoperative and 396 +/- 15 vs. 320 +/- 12 msec, p less than 0.001, postoperative). Changes in DT after propranolol are mainly attributed to decreased HR. Changes in QS2 were much less profound and always less (p less than 0.01) than changes in DT. Thus propranolol significantly increased DT per beat in patients with coronary artery disease, which allowed more time for coronary perfusion; this effect of propranolol could well be as important as the reduction of myocardial oxygen consumption.
舒张期时间（DT）通过心动周期长度减去机电收缩期（QS2）计算得出，它与心率（HR）呈非线性关系，当心率降至75次/分钟以下时，舒张期时间会迅速增加。在150例冠心病患者中研究了普萘洛尔对舒张期时间的影响。患者被分为三组。第一组包括稳定型心绞痛患者：在第一组的23例患者中，静脉注射普萘洛尔（2.5毫克）使舒张期时间从411±18毫秒显著增加至527±22毫秒（p＜0.001）；在15例稳定型心绞痛患者中，使用普萘洛尔治疗（平均每日剂量200±15毫克）使舒张期时间从446±29毫秒增加至766±26毫秒（p＜0.001）。第二组由急性心肌梗死患者组成：在其中18例患者中，静脉注射普萘洛尔（2.5毫克）使舒张期时间从379±16毫秒增加至458±24毫秒（p＜0.001）。第三组包括近期接受冠状动脉搭桥手术的患者：在术后7天，14例患者静脉注射普萘洛尔（2.5毫克）使舒张期时间从323±9毫秒增加至468±24毫秒（p＜0.001）。此外，比较了30例持续使用普萘洛尔（术前平均每日剂量155±11毫克，术后68±9毫克）的患者与50例未使用普萘洛尔接受冠状动脉搭桥手术的其他患者术后15小时和2周时的舒张期时间。使用普萘洛尔的患者舒张期时间更长（术前546±21毫秒对388±16毫秒，p＜0.001；术后396±15毫秒对320±12毫秒，p＜0.001）。普萘洛尔治疗后舒张期时间的变化主要归因于心率降低。机电收缩期（QS2）的变化程度要小得多，且始终小于舒张期时间的变化（p＜0.01）。因此，普萘洛尔可显著增加冠心病患者的每搏舒张期时间，从而为冠状动脉灌注留出更多时间；普萘洛尔的这一作用可能与降低心肌耗氧量同样重要。
