PARASYMPATHETIC NEURONS IN THE CRANIAL MEDIAL VENTRICULAR FAT PAD ON THE DOG HEART SELECTIVELY DECREASE VENTRICULAR CONTRACTILITY

We hypothesized that selective control of ventricular contractility mi ght be mediated by postganglionic parasympathetic neurons in the crani al medial ventricular (CMV) ganglion plexus located in a fat pad at th e base of the aorta. Sinus rate, atrioventricular (AV) conduction (ven tricular rate during atrial pacing), and left ventricular contractile force (LV dP/dt during right Ventricular pacing) were measured in eigh t chloralose-anesthetized dogs both before and during bilateral cervic al vagus stimulation (20-30 V, 0.5 ms pulses. 15-20 Hz). Seven of thes e dogs were tested under beta-adrenergic blockade (propranolol, 0.8 mg kg(-1) i.v.). Control responses included sinus node bradycardia or ar rest during spontaneous rhythm, high grade AV block or complete heart block, and a 30% decrease in contractility from 2118 +/- 186 to 1526 /- 187 mm Hg s(-1) (P < 0.05). Next, the ganglionic blocker trimethaph an (0.3-1.0 ml of a 50 mu g ml(-1) solution) was injected into the CMV fat pad. Then vagal stimulation was repeated, which now produced a re latively small 5% (N.S., P > 0.05) decrease in contractility but still elicited the same degree of sinus bradycardia and AV block (N = 8, P < 0.05). Five dogs were re-tested 3 h after trimethaphan fat pad injec tion, at which time blockade of vagally-induced negative inotropy was partially reversed, as vagal stimulation decreased LV dP/dt by 19%. Th e same dose of trimethaphan given either locally into other fat pads ( PVFP or IVC-ILA) or systemically (i.v.) had no effect on vagally-induc ed negative inotropy. Thus, parasympathetic ganglia located in the CMV fat pad mediated a decrease in ventricular contractility during vagal stimulation. Blockade of the CMV fat pad had no effect on vagally-med iated slowing of sinus rate or AV conduction. (C) 1998 Published by El sevier Science B.V. All rights reserved.