Vormittag E, Keiler A
Arzneimittelforschung. 1979;29(10):1534-8.
Effects of beta-receptor blockade by oxprenolol, which significantly prevented subendocardial necroses during hemorrhagic shock in dogs, on shock tolerance and myocardial function were analyzed. Overall mortality was not altered by beta-receptor blockade. Cardiac output and contractility (dp/dtmax) before, during and after a hypovolemic period of 120 to 210 min with mean arterial pressure = 40 +/- 5 mmHg showed no significant difference with or without oxprenolol treatment. Increase of heart rate during hemorrhage was abolished completely by oxprenolol and as a consequence of this duration of the diastolic filling period was about three times longer (p less than 0.001) and stroke volumes were greater. Stress metabolism was improved. Hyperglycemia and metabolic acidosis were diminished and arterial oxygen tension was higher in the treated group. Incidence of lethal ventricular fibrillation was higher and pulsus alternans found only in the control group. The beneficial effects of beta-receptor blockage on the course of hemorrhagic shock are explained by the prevention of the catecholamine induced tachycardia and thereby increased coronary perfusion and decreased myocardial oxygen consumption and by the intrinsic sympathicomimetic activity of oxprenolol.