Bodenheimer M M, Banka V S, Helfant R H
Am Heart J. 1976 Oct;92(4):481-6. doi: 10.1016/s0002-8703(76)80048-8.
Recent studies have suggested that propranolol decreases the extent of myocardial injury in acute ischemia. Although other studies have shown that global myocardial performance is depressed, zonal effects of propranolol in this setting are unknown. Therefore, the effect of propranolol (1.0 mg. per kilogram) was investigated in nine dogs with the use of Walton-Brodie strain gauge arches and local epicardial electrograms (10 to 12 sites). The heart rate effects of propranolol were controlled by atrial pacing. After coronary occlusion, heart rate increased slightly without a significant change in blood pressure. Following the infusion of propranolol, heart rate decreased significantly from 165.0 +/- 3.5 to 126.2 +/- 4.7 beats per minute (p less than 0.001) while both the systolic and diastolic blood pressures showed insignificant changes. After coronary occlusion, nonischemic zone tension showed no significant changes; however, propranolol decreased total tension from 105.2 +/- 2.5 per cent to 66.8 +/- 4.7 (p less than 0.001). Similarly, propranolol further decreased total tension in the border zone from 84.4 +/- 6.7 per cent (p less than .02) to 50.6 +/- 5.1 (p less than 0.01). Ischemic zone tension also fell further (p less than 0.025) after propranolol. Restoration of prepropranolol heart rate had no significant effect on tension development. Following coronary occlusion, sigmaST increased from 5.7 +/- 2.2 to 72.9 +/- 20.1 mv. (p less than 0.001). Coincident with the decrease in heart rate and tension development induced by propranolol, sigmaST decreased to 60.8 +/- 18.8 mv. (p less than 0.05). When the heart rate was restored to prepropranolol level, sigmaST again rose to 73.2 +/- 16.9 mv. (p less than .005). Thus, propranolol does effect an improvement in ischemic injury which is related, at least in part, to the induced decrease in heart rate. A concomitant substantial decrease in local tension development also occurs, however. The latter observations may limit the potential usefulness of propranolol in this setting.
近期研究表明,普萘洛尔可减轻急性缺血时心肌损伤的程度。尽管其他研究显示整体心肌功能会受到抑制,但普萘洛尔在此情况下的局部作用尚不清楚。因此,利用沃尔顿 - 布罗迪应变片式心腔大小测定器和局部心外膜电图(10至12个部位),对9只犬进行了普萘洛尔(每千克1.0毫克)作用的研究。普萘洛尔对心率的影响通过心房起搏来控制。冠状动脉闭塞后,心率略有增加,血压无显著变化。输注普萘洛尔后,心率从每分钟165.0±3.5次显著降至126.2±4.7次(p<0.001),而收缩压和舒张压均无明显变化。冠状动脉闭塞后,非缺血区张力无显著变化;然而,普萘洛尔使总张力从105.2±2.5%降至66.8±4.7%(p<0.001)。同样,普萘洛尔使边缘区总张力从84.4±6.7%(p<0.02)进一步降至50.6±5.1%(p<0.01)。普萘洛尔应用后,缺血区张力也进一步下降(p<0.025)。恢复普萘洛尔应用前的心率对张力发展无显著影响。冠状动脉闭塞后,∑ST从5.7±2.2增加至72.9±20.1毫伏(p<0.001)。与普萘洛尔引起的心率和张力发展降低相一致,∑ST降至60.8±18.8毫伏(p<0.05)。当心率恢复到普萘洛尔应用前水平时,∑ST再次升至73.2±16.9毫伏(p<0.005)。因此,普萘洛尔确实能改善缺血性损伤,这至少部分与诱导的心率降低有关。然而,同时局部张力发展也会大幅下降。后一观察结果可能会限制普萘洛尔在此情况下的潜在用途。