Altered nicotinic sensitivity of AV node in surgically denervated canine hearts.
The responses of normal and cardiac-denervated (DNV) dogs to acetylcholine (ACh) and nicotine (NIC) were examined to determine if the intrinsic cardiac nerves (ICN) that modulate electrical conduction display denervation supersensitivity. Control (n = 18) and DNV (n = 18) animals were placed on cardiopulmonary bypass. Recording of intra-atrial (P-A), intraventricular (H-V), and atrioventricular (AV) nodal (A-H) conduction times were made from the region of the His bundle. ACh (0.1-10 micrograms) was used to produce muscarinic stimulation, whereas NIC (0.1-400 micrograms) was employed to stimulate the ICN. All drugs were administered intracoronary. No supersensitivity to either ACh or NIC was seen in the data from the P-A or H-V intervals of the His electrogram in the DNV animals. However, this group displayed approximately a 10-fold increase in the negative dromotropic effect of NIC on the AV node compared with control. No significant change in muscarinic sensitivity of the AV node was observed in the DNV animals. We conclude that 1) no denervation supersensitivity of the ICN mediating effects on intra-atrial and intraventricular conduction occurs; 2) the AV node itself does not show muscarinic supersensitivity following extrinsic denervation; 3) the ICN do display denervation supersensitivity as shown by a 10-fold increase in the effects of NIC on AV nodal conduction time.
D000109:Acetylcholine / Q000494:pharmacology*; D000818:Animals; D001283:Atrioventricular Node / Q000187:drug effects / Q000502:physiology*; D003714:Denervation; D004285:Dogs; D004305:Dose-Response Relationship, Drug; D004553:Electric Conductivity; D006329:Heart Conduction System / Q000502:physiology*; D009538:Nicotine / Q000494:pharmacology*; D013779:Tetrodotoxin / Q000494:pharmacology
D013779:Tetrodotoxin; D009538:Nicotine; D000109:Acetylcholine