title: Cardiac effects induced by chemically activated neurons in canine intrathoracic ganglia.
abstract: 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.
authors.affiliation: Department of Surgery, Faculty of Medicine, Dalhousie University, Halifax, Nova Scotia, Canada.
authors.forename: C K
authors.initials: CK
authors.lastname: Butler
authors.forename: F M
authors.initials: FM
authors.lastname: Smith
authors.forename: J
authors.initials: J
authors.lastname: Nicholson
authors.forename: J A
authors.initials: JA
authors.lastname: Armour
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000596:Amino Acids / Q000494:pharmacology; D000818:Animals; D004285:Dogs; D005260:Female; D005724:Ganglia / Q000187:drug effects / Q000502:physiology*; D006321:Heart / Q000502:physiology*; D007267:Injections; D007545:Isoproterenol / Q000494:pharmacology; D008297:Male; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D009538:Nicotine / Q000494:pharmacology; D013909:Thorax / Q000294:innervation
chemical_list: D000596:Amino Acids; D009538:Nicotine; D007545:Isoproterenol; D000109:Acetylcholine