Abstract
1 Cardiac anaphylaxis and the effects of glucagon pretreatment were studied in guinea-pig isolated hearts actively sensitized to ovalbumin.2 Antigen challenge of the sensitized hearts markedly increased creatine phosphokinase (CPK) activity in the coronary venous effluent. Control values of CPK release from the hearts before challenge were 3.56 +/- 0.15 mu min(-1) mg(-1). In the first 10 min following challenge, CPK release remained stable at increased levels which ranged between 4.88 +/- 0.20 to 5.39 +/- 0.38 mu min(-1) mg(-1). There was no correlation between immunologically released histamine and CPK release.3 Pretreatment of the hearts with glucagon (0.15 mumol l(-1)) exerted a pronounced anti-arrhythmic activity, reducing the conduction arrhythmias and completely preventing automaticity arrhythmias which normally occurred following ovalbumin challenge.4 Anaphylactic histamine release was reduced significantly in the presence of glucagon. The percentage inhibition of histamine release from glucagon pretreated hearts, during the first 10 min after challenge, ranged between 58% and 94% of that from hearts similarly challenged in the absence of glucagon.5 Glucagon significantly elevated sinoatrial nodal automaticity, enhanced atrioventricular conduction, improved coronary flow and reduced contractile force during anaphylaxis. It appears that these effects are caused both by modulating anaphylactic histamine release and by influencing the effects of the released histamine.6 CPK release from the anaphylactic hearts was significantly inhibited in the presence of glucagon. The average percentage inhibition of CPK activity during the first 10 min after challenge ranged between 42% and 98%.7 The findings from this study provide experimental evidence for protective effects of glucagon pretreatment during cardiac anaphylaxis.