VAGAL CONTROL OF LEFT-VENTRICULAR CONTRACTILITY IS SELECTIVELY MEDIATED BY A CRANIOVENTRICULAR INTRACARDIAC GANGLION IN THE CAT

Activation of the vagus nerve leads to decreases in sinoatrial (SA) ra te, atrioventricular (AV) conduction, and myocardial contractility. Pr evious data are consistent with the hypothesis that vagal control of c ardiac rate and AV conduction are mediated by two anatomically separat ed and physiologically independent parasympathetic intracardiac gangli a located in fat pads on the surface of the right and left atria, resp ectively. These data suggested that vagal control of ventricular contr actility might be mediated through another intracardiac ganglion. We e xamined the ventricles of cat hearts histologically for the presence o f ganglia. Multiple small basophilic ganglia composed of a few neurons , and an occasional larger ganglion were found embedded in the epicard ial fat surrounding the cranial margin of the anterior surface of the left ventricle, near the juncture with the right ventricle, which we r efer to as the CV ganglion. In anesthetized cats, right cervical vagal stimulation decreased SA rate by 44 +/- 5%, decreased the rate of AV conduction by 68 +/- 14%, and reduced ventricular contractility by 19. 5 +/- 5.7%. Vagally induced negative inotropism was almost completely prevented by microinjection of a ganglionic blocking drug into the CV ganglion. However, these injections into the CV ganglion did not signi ficantly effect vagally induced decreases in either SA rate or AV cond uction. We conclude: (1) that ganglia are found in a fat pad on the su rface of the left ventricle of the cat heart and (2) that the CV gangl ion selectively mediates the negative inotropic effect of vagal stimul ation on the left ventricle. Greater understanding of the physiologica l functions of intracardiac neuronal circuits may help in developing n ew strategies to treat disorders of cardiac contractility such as cong estive heart failure. (C) 1997 Elsevier Science B.V.