Anesthetics and automaticity of dominant and latent atrial pacemakers in chronically instrumented dogs. III. Automaticity after sinoatrial node excision.
BACKGROUND
Management of patients with sinus node dysfunction must consider the stability of subsidiary pacemakers during anesthesia and treatment with antimuscarinic or sympathomimetic drugs. Baroreflex regulation of atrial pacemaker function is known to contribute to the interactions between inhalation anesthetics and catecholamines. Sinoatrial (SA) node excision can be a model for intrinsic SA node dysfunction. Subsidiary atrial pacemakers are expected to emerge after SA node excision, but they may respond differently to humoral and neural modulation. Isolated and combined effects of epinephrine and methylatropine should help characterize subsidiary pacemaker function during anesthesia with halothane, isoflurane, and enflurane.


METHODS
In eight dogs, SA nodes were excised and epicardial electrodes implanted at the atrial appendages, the His bundle, and along the sulcus terminalis. Spontaneous pacemaker automaticity and subsidiary atrial pacemaker recovery time were measured in the conscious state, in the presence of methylatropine, with 1 and 2 micrograms.kg-1.min-1 epinephrine and during 1.25 and 2 MAC halothane, isoflurane, and enflurane.


RESULTS
After SA node excision, a stable and regular subsidiary atrial pacemaker rhythm emerged. Each anesthetic prolonged subsidiary atrial pacemaker recovery times. This prolongation was greater in the presence of methylatropine. Without methylatropine, isoflurane and enflurane, but not halothane, further enhanced the baroreflex-mediated negative chronotropic effects of epinephrine, whereas with methylatropine, each anesthetic reduced the direct positive chronotropic effects of epinephrine.


CONCLUSIONS
Halothane, isoflurane, and enflurane have significant depressant effects on the spontaneous and epinephrine-altered automaticity of subsidiary atrial pacemakers. Depression of subsidiary atrial pacemaker automaticity was most apparent in dogs with muscarinic blockade.
Vicenzi
M N
MN
Department of Anesthesiology, Medical College of Wisconsin, Milwaukee 53226.
Woehlck
H J
HJ
Bajic
J
J
Sokolyk
S M
SM
Bosnjak
Z J
ZJ
Atlee
J L
JL
D000777:Anesthetics / Q000494:pharmacology*; D000818:Animals; D016275:Atrial Function; D001286:Atropine Derivatives / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects; D004285:Dogs; D004737:Enflurane / Q000494:pharmacology; D004837:Epinephrine / Q000494:pharmacology; D006221:Halothane / Q000494:pharmacology; D006339:Heart Rate / Q000187:drug effects*; D007530:Isoflurane / Q000494:pharmacology; D012849:Sinoatrial Node / Q000502:physiology* / Q000601:surgery
D000777:Anesthetics; D001286:Atropine Derivatives; C006649:methylatropine; D004737:Enflurane; D007530:Isoflurane; D006221:Halothane; D004837:Epinephrine