CHEMICAL MODULATION OF IN-SITU INTRINSIC CARDIAC NEURONS INFLUENCES MYOCARDIAL BLOOD-FLOW IN THE ANESTHETIZED DOG

Objective: The aim was to determine whether modulation of intrinsic ca rdiac neurones influences the distribution of myocardial blood flow in canine anaesthetised open chest experimental preparations. Methods: I ntrinsic cardiac neurones were modified by locally applied nicotine (1 00 mu g) or bradykinin (50 mu g) while changes were recorded in cardia c haemodynamics and myocardial blood flow (radiolabelled microspheres) . Right acid left ventricular intramyocardial tissue pressures were me asured with high fidelity microtip transducers. Results: Control injec tions of saline (vehicle; 0.1 ml) into active loci did not produce car diovascular responses. Nicotine modulation of intrinsic cardiac neuron es did not change coronary artery conductance, but total myocardial bl ood flow [116(SEM 17) v 532(97) ml.min(-1).100 g(-1),; p = 0 001 v bas eline] and oxygen consumption [7.92(1.10) v 20.14(1.86) ml min(-1).100 g(-1); p = 0.001] increased in direct relation to heart rate-blood pr essure product changes. Locally administered bradykinin increased coro nary artery conductance [2.62(0.39) v 4.71(1.07) ml.min(-1).100 g(-1). mm Hg-1], total myocardial blood flow, to 263(72) ml.min(-1).100 g(-1) , and oxygen consumption, to 14.9(4.4) ml.min(-1).100 g(-1); however, heart rate-blood pressure product did not change. Conclusions: These r esults support earlier findings that intrinsic neurones are involved i n cardiac regulation. Furthermore, modification of intrinsic cardiac n eurones by nicotine or bradykinin significantly alters the distributio n of myocardial blood flow, possibly because of increased myocardial m etabolism.