The cardiodynamic and metabolic effects of carbochromen and propranolol on the isolated dog heart.

In the isolated canine heart-lung preparation modified to measure coronary outflow and myocardial oxygen consumption, an infusion of carbochromen of 1 mg/min produced an increase in coronary outflow of 120.0% and a decrease in myocardial oxygen consumption of 11.0% at a cumulative dose of 28.0 +/- 3.8 mg, resulting in an increase in efficiency of 22.4%. At a total dose of 40 mg, the corresponding figures were +181.0%, -15.0% and +38.0% respectively. No change in heart rate was observed. An infusion of propranolol of 1 mg/min, on the other hand, was characterized by decreases in myocardial contractility and heart rate starting with cumulative doses of 20 mg and 40 mg respectively. At a cumulative dose of 62.9 +/- 3.0 mg a marked degree of myocardial failure occurred (peak failure) characterized by a decrease in cardiac output (-53.3%), dp/dt (-50.8%), heart rate (-18.5%) and myocardial oxygen consumption (-25.5%). In a separate series exposed to the same infusion of propranolol but in which the decrease in heart rate was prevented by pacing, identical changes were observed except that myocardial oxygen consumption decreased only by 7.7%. It may be concluded from this study that carbochromen, in confirmation of reports by other investigators, increases coronary outflow markedly. Carbochromen decreases myocardial oxygen consumption by a direct effect on myocardial metabolism as is evident from the fact that this decrease is not accompanied by changes in any of the parameters which are known to influence myocardial oxygen consumption such as heart rate. Propranolol has no effect on myocardial oxygen consumption unless it is given in a dose which produces myocardial failure and a decrease in heart rate. The decrease in heart rate following propranolol bears a close relationship to the decrease in myocardial oxygen consumption.