Hattori S, Banka V S, Agarwal J B, Yamazaki H, Bodenheimer M M, Helfant R H
Am J Cardiol. 1982 Sep;50(3):478-82. doi: 10.1016/0002-9149(82)90312-5.
Use of propranolol in acute myocardial infarction is limited by its cardiodepressant effects. The effects of nitroglycerin (0.4 mg intravenously) on regional myocardial dysfunction produced by total or partial (50 percent) coronary occlusion and intravenous administration of propranolol (1.0 mg/kg) were evaluated using pairs of ultrasonic crystals implanted subendocardially in the nonischemic and ischemic zones in 14 open chest dogs. During partial coronary occlusion, systolic shortening (% delta L) in the ischemic zone decreased from 20.9 +/- 5.3 to 7.2 +/- 6.4 (p less than 0.001). Propranolol did not change it significantly. Nitroglycerin increased % delta L from 6.7 +/- 4.5 to 11.2 +/- 5.3 (p less than 0.01). The nonischemic zone was unaffected by partial coronary occlusion but showed a decrease in % delta L from 18.6 +/- 6.2 to 15.6 +/- 5.1 (p less than 0.01) with propranolol. Nitroglycerin increased % delta L from 15.6 +/- 5.1 to 17.3 +/- 5.9 (p less than 0.02). During total coronary occlusion, nitroglycerin administration after propranolol improved % delta L in the nonischemic but not in the ischemic zone. Nitroglycerin caused a significant decrease in left ventricular systolic and end-diastolic pressures. Heart rate remained unchanged. It is concluded that nitroglycerin reversed myocardial depressant effects of propranolol in both the partially ischemic and the nonischemic zones after acute coronary occlusion.