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Notes: Summary In 7 healthy-hearted probands the arterial-coronary-venous oxygen difference for glucose, K+, lactate, pO2, pCO2 and pH during a glucagon infusion was determined and compared with the values before and 10 minutes after infusion. Contradictory to the unchanged myocardial lactate extraction and the positively or negatively influenced K+-uptake recorded in the literature, in this contingent there was a statistically significant myocardial lactate production and an unchanged potassium uptake. The respiratory quotient of the heart increased. These changes are regarded as the result of a direct hormonal influence on the myocardial metabolism and have nothing to do with the change of an aerobic into an anaerobic metabolic state.

Notes: Summary In the cases of 10 cardially healthy humans and 5 patients with heart disease, the left ventricular pressure as well as different parameters of contractility-deduced from the pressure curve and its first derivative-were determined by a catheter-tip manometer (Statham SF-1). In particular the following values were concerned: dP/dtmax,dP/dtmax/DP, the maximal calculated shortening velocity of the contractile elements according to the 2-component heart muscle model (VCEmaxTP) as well as with the Maxwell model (VCEmaxDP) and finally the (extrapolated) maximum shortening velocity (Vmax) under a fictive zero load. The examinations were carried out before and during a 10-minute infusion of 60 mg/kg glucagon and 10 minutes after completing the infusion. Besides glucagon also digoxin, etilefrin·HCl1) and orciprenaline2) were delivered and the same measurements were performed as with glucagon. A definite statement about the priority of any one of the named indices of contractility is rendered more difficult, because the enddiastolic pressure does not change substantially with glucagon. An unequivocal demarcation of frequency and pressure effects and of inotropic mechanisms as just as impossible, because, with the exception of VmaxDP, all parameters react quantitatively and qualitatively in an equal manner. On the basis of VmaxTP the result of glucagon is only a slight increase in the myocardial contractile capability, which would hardley suffice for the treatment of patients, who do not respond to digitalis. The decline of VmaxDP under glucagon cannot be explained. Under digitalis, etilefrin and orciprenaline, a similar dissociation of values for the maximum shortening velocity according to the 2- or 3-component-model of the heart muscle cannot be demonstrated. Das Ausmaß der Veränderungen der linksventrikulären Dynamik des menschlichen Herzens unter Glukagonwirkung wird in der Literatur sehr verschieden beurteilt. Da hierfür möglicherweise unterschiedliche Meßverfahren für die Bestimmung der Kontraktilitätsparameter ursächlich in Frage kommen, wurde auf die Bestimmung der “maximalen Geschwindigkeit der lastfreien Verkürzung der kontraktilen Elemente (Vmax) besonderer Wert gelegt. In den bisher vorliegenden Arbeiten (siehe Diskussion) wurde diese Größe zur Beurteilung der inotropen Glukagonwirkung am menschlichen Herzen in situ noch nicht berücksichtigt. Für Vmax ergeben sich differente Werte je nach Anwendung des 2- oder 3-Komponenten-Herzmuskelmodells. Die Aussagekraft von Vmax wurde ferner durch Vergleich mit den bisher bereits unter Glukagon gemessenen Kontraktilitätsparametern (dP/dtmax, dP/dtmax/DP sowie VCEmax [in der Literatur auch als Vpeak measured bezeichnet]) abzugrenzen versucht (Tab. 1a). Außerdem wurde die Glukagonwirkung dem positiv inotropen Effekt anderer Pharmaka gegenübergestellt.