Activity of in vivo atrial and ventricular neurons in chronically decentralized canine hearts.

The spontaneous activity of 175 neurons located in the ventral right atrial and ventral interventricular ganglionated plexi was recorded in eight anesthetized dogs, the hearts of which were chronically decentralized at least 2 wk before recordings were made. Ganglia were subsequently identified anatomically in the immediate vicinity of the recording sites. Spontaneous activity was correlated with the cardiac cycle in 57% of the atrial and 62% of the ventricular neurons and with the respiratory cycle in 29% of the atrial and 28% of the ventricular neurons. Spontaneous cardiovascular-related activity was recorded when systemic arterial pressure was between 80 and 175 mmHg. The activity of 23 atrial and 15 ventricular neurons was altered when discrete regions of the heart were mechanically distorted by gentle touch. These data imply that cardiac ganglionated plexi contain afferent neurons that receive inputs from limited regions of the heart. The spontaneous activity generated by intracardiac neurons was not altered when extracardiac tissues were distorted. These results demonstrate that neurons in ganglia on chronically decentralized hearts can generate spontaneous activity, a large fraction of which is correlated with cardiovascular or respiratory events.

Cardiac responses to electrical stimulation of discrete loci in canine atrial and ventricular ganglionated plexi.

The purpose of the present study was to examine cardiac effects induced by electrical stimulation (1-4 V, 1 ms, 200 Hz) of discrete loci within the ganglionated plexi located on canine atria and ventricles. When 20 loci in the right atrial ventral ganglionated plexi of 11 anesthetized open-chest dogs were stimulated, bradycardia and/or right and left atrial force suppression occurred when, on average, 15% of these loci were stimulated. Bradycardia and atrial force suppression were elicited when, on average, 8% of 15 loci in the left atrial ventral ganglionated plexi of eight dogs was stimulated. When these loci were restimulated after acute decentralization, cardiac responses were attenuated or occasionally eliminated. After atropine (1 mg/kg iv) administration, repeat stimulation of loci in the right but not left atrial ganglionated plexus induced tachycardia. Stimulation of loci in the right ventricular ganglionated plexus after the subsequent administration of desipramine (1 mg/kg iv) in six dogs resulted in an increase in right ventricular conus intramyocardial pressure. After hexamethonium administration (10 mg/kg iv, followed by a continuous infusion of 1 mg.kg-1.min-1), sympathetic responses were no longer elicited from one of the five dogs in which loci in the right atrial ganglionated plexi and from two of the six dogs in which loci of the right ventricular ganglionated plexus had elicited responses. We conclude that atrial and ventricular ganglionated plexi contain efferent parasympathetic, efferent sympathetic, and afferent neurons.

Cardiac effects induced by chemically activated neurons in canine intrathoracic ganglia.

Regional or global cardiac responses were elicited when various chemicals were injected into discrete loci within acutely decentralized stellate and middle cervical ganglia. Nicotine (100 micrograms), acetylcholine (100 micrograms), or isoproterenol (1, 2, or 5 micrograms) in 1 microliters of normal saline was administered individually into 30 discrete loci within each stellate ganglion and 25 within each middle cervical ganglion. Cardiac augmentation was elicited when approximately 1 site per ganglion was injected with nicotine or acetylcholine. Similar injections into sites approximately 1-2 mm away from an active site usually failed to elicit cardiac responses. Isoproterenol elicited cardiac augmentations when injected into, on average, 3 different loci per ganglion. The responses elicited by isoproterenol injections were eliminated when the efferent sympathetic nerves arising from an injected ganglion were divided or when timolol maleate (0.1 mg/microliters normal saline) was previously injected into the same locus. These data indicate that the effects elicited by injecting isoproterenol into an intrathoracic ganglion locus were not due to leakage of this agent into the blood in sufficient quantities to directly activate cardiac myocytes. When L-glutamic acid (100 microliters of 1 M solution in normal saline) or L-aspartic acid (100 microliters of 1 M solution in normal saline) was injected into a stellate ganglion or middle cervical ganglion, positive chronotropic and/or inotropic responses were elicited. When DL-homocysteic acid (100 microliters of 1 M solution in normal saline) was administered no augmentation occurred. It is concluded that intrathoracic ganglion cardiac neurons can be activated by nicotinic or beta-adrenergic agonists, as well as by specific amino acids. These neurons are located throughout the stellate and middle cervical ganglia, cardiac neurons in one ganglionic locus being capable of activation by more than one of these chemicals.

Modification of supraventricular tachyarrhythmias by stimulating atrial neurons.

The effects of stimulating the right atrial ventral ganglionated plexus on ventricular performance during atrial tachycardia was studied in 8 lightly sedated (pentobarbital, 2.5 mg/kg intravenously) dogs with sterile pericarditis. Atrial arrhythmias were induced by electrical stimulation (10 V, 4 ms, 100 Hz) of the right atrium through previously inserted temporary bipolar pacemaker wires. Various types of supraventricular tachycardias were produced. Atrial fibrillation was produced in 3 dogs, atrial tachycardia in all 8 dogs, different atrioventricular nodal ectopic rhythms in 6 dogs, and atrial flutter in 1 dog. These arrhythmias were associated with irregular ventricular contractions that resulted in low ventricular pressures during many cardiac cycles such that low or no aortic pressure was generated. Right atrial ventral ganglionated plexus stimulation induced slowing of ventricular rate so that every ventricular contraction resulted in aortic pressure generation, thus increasing mean aortic pressure. Responses elicited by atrial ganglionated plexus stimulation were eliminated after atropine administration. We conclude that electrical stimulation of the right atrial ventral ganglionated plexus results in slowing of ventricular contractile rate during supraventricular tachycardia, presumably by activating efferent vagal neuronal elements, thereby improving ventricular performance. If applicable in humans, this technique may be of use in management of postoperative atrial arrhythmias after cardiac operations.

Cardiac responses elicited by peptides administered to canine intrinsic cardiac neurons.

In order to study the effects of peptides on intrinsic cardiac neurons, substance P, bradykinin, oxytocin, calcitonin gene related peptide, atrial natriuretic peptide and vasoactive intestinal peptide were administered into canine atrial or ventricular ganglionated plexi. When substance P was injected into right atrial or cranial medial ventricular ganglionated plexi heart rate, atrial force and ventricular intramyocardial pressures were augmented. No cardiac changes occurred when similar volumes of saline (i.e., peptide vehicle) were injected into these ganglionated plexi. When bradykinin was injected into atrial or ventricular ganglionated plexi heart rate, atrial force and ventricular force were augmented in approximately 50% and depressor responses were elicited in approximately 50% of these animals. When oxytocin was injected into right atrial ventral ganglionated plexi heart rate and atrial forces were reduced in five of ten dogs studied. No cardiac changes occurred when oxytocin was injected into left atrial or ventricular ganglionated plexi. No responses were elicited when calcitonin gene related peptide, atrial natriuretic peptide or vasoactive intestinal peptide was administered into atrial or ventricular ganglionated plexi. Following acute decentralization of the heart, no significant responses were elicited by repeat administrations of substance P, bradykinin or oxytocin, implying that connectivity with central nervous system neurons was necessary for consistent responses to be elicited. It is concluded that substance P, bradykinin and oxytocin can affect neurons on the heart such that cardiodynamics are modified, these different peptides eliciting different cardiac responses.

Systolic pressure gradients between the wall of the left ventricle, the left ventricular chamber, and the aorta during positive inotropic states: implications for left ventricular efficiency.

To study systolic pressure gradients developed between the left ventricular wall, its chamber, and the aortic root, in one group of dogs left ventricle ventral wall intramyocardial pressure, left ventricular outflow tract pressure, and aorta pressure were compared with aortic flow as well as left ventricular dimension changes during control conditions as well as during positive intropic states induced by isoproterenol, stellate ganglion stimulation, and noradrenaline. In another group of dogs systolic pressures in the ventral wall of the left ventricle, the main portion of the left ventricular chamber, and the aorta were compared with aortic flow during similar interventions, before and after the administration of phentolamine. Pressure gradients between the wall of the left ventricle and the outflow tract of the left ventricle were minimal during control states, but during the three positive inotropic states were increased significantly. In contrast, pressure gradients between the outflow tract of the left ventricle and the aortic root were insignificant during positive inotropic states; those between the wall and main portion of the chamber were only significantly different during left stellate ganglion stimulation. The data derived from these experiments indicate that useful peak power output of the left ventricle (systolic aortic pressure X flow) is unchanged following isoproterenol infusion, but is increased by stellate ganglion stimulation and noradrenaline. The useful peak power output index (an index of left ventricular efficiency derived by dividing useful peak power output by peak intramyocardial pressure) was reduced more by isoproterenol than the other two interventions.(ABSTRACT TRUNCATED AT 250 WORDS)