title: Activated cranial cervical cord neurons affect left ventricular infarct size and the potential for sudden cardiac death.
abstract: To evaluate whether cervical spinal neurons can influence cardiac indices and myocyte viability in the acutely ischemic heart, the hearts of anesthetized rabbits subjected to 30 min of LAD coronary arterial occlusion (CAO) were studied 3h after reperfusion. Control animals were compared to those exposed to pre-emptive high cervical cord stimulation (SCS; the dorsal aspect of the C1-C2 spinal cord was stimulated electrically at 50 Hz; 0.2 ms; 90% of motor threshold, starting 15 min prior to and continuing throughout CAO). Four groups of animals were so tested: 1) neuroaxis intact; 2) prior cervical vagotomy; 3) prior transection of the dorsal spinal columns at C6; and 4) following pharmacological treatment [muscarinic (atropine) or adrenergic (atenolol, prazosin or yohimbine) receptor blockade]. Infarct size (IS) was measured by tetrazolium, expressed as percentage of risk zone. C1-C2 SCS reduced acute ischemia induced IS by 43%, without changing the incidence of sudden cardiac death (SCD). While SCS-induced reduction in IS was unaffected by vagotomy, it was no longer evident following transection of C6 dorsal columns or atropinization. Beta-adrenoceptor blockade eliminated ischemia induced SCD, while alpha-receptor blockade doubled its incidence. During SCS, myocardial ischemia induced SCD was eliminated following vagotomy while remaining unaffected by atropinization. These data indicate that, in contrast to thoracic spinal neurons, i) cranial cervical spinal neurons affect both adrenergic and cholinergic motor outflows to the heart such that ii) their activation modifies ventricular infarct size and lethal arrhythmogenesis.
authors.affiliation: Department of Pharmacology, East Tennessee State University, Johnson City, TN, United States.
authors.forename: E Marie
authors.initials: EM
authors.lastname: Southerland
authors.forename: David D
authors.initials: DD
authors.lastname: Gibbons
authors.forename: S Brooks
authors.initials: SB
authors.lastname: Smith
authors.forename: Adam
authors.initials: A
authors.lastname: Sipe
authors.forename: Carole Ann
authors.initials: CA
authors.lastname: Williams
authors.forename: Eric
authors.initials: E
authors.lastname: Beaumont
authors.forename: J Andrew
authors.initials: JA
authors.lastname: Armour
authors.forename: Robert D
authors.initials: RD
authors.lastname: Foreman
authors.forename: Jeffrey L
authors.initials: JL
authors.lastname: Ardell
mesh_terms: D059331:Adrenergic Neurons / Q000187:drug effects / Q000502:physiology; D000317:Adrenergic alpha-Antagonists / Q000009:adverse effects; D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000818:Animals; D002574:Cervical Vertebrae; D059329:Cholinergic Neurons / Q000187:drug effects / Q000502:physiology; D054059:Coronary Occlusion / Q000503:physiopathology; D003391:Cranial Nerves / Q000187:drug effects / Q000502:physiology* / Q000601:surgery; D016757:Death, Sudden, Cardiac / Q000209:etiology / Q000517:prevention & control*; D003714:Denervation; D004195:Disease Models, Animal; D004599:Electric Stimulation Therapy; D005260:Female; D006352:Heart Ventricles / Q000187:drug effects / Q000294:innervation / Q000473:pathology; D008297:Male; D009203:Myocardial Infarction / Q000473:pathology*; D017202:Myocardial Ischemia / Q000209:etiology / Q000473:pathology / Q000503:physiopathology / Q000628:therapy*; D011817:Rabbits; D012306:Risk; D013116:Spinal Cord / Q000187:drug effects / Q000502:physiology* / Q000601:surgery
chemical_list: D000317:Adrenergic alpha-Antagonists; D000319:Adrenergic beta-Antagonists