title: Paraplegia increased cardiac NGF content, sympathetic tonus, and the susceptibility to ischemia-induced ventricular tachycardia in conscious rats.
abstract: Midthoracic spinal cord injury is associated with ventricular arrhythmias that are mediated, in part, by enhanced cardiac sympathetic activity. Furthermore, it is well known that sympathetic neurons have a lifelong requirement for nerve growth factor (NGF). NGF is a neurotrophin that supports the survival and differentiation of sympathetic neurons and enhances target innervation. Therefore, we tested the hypothesis that paraplegia is associated with an increased cardiac NGF content, sympathetic tonus, and susceptibility to ischemia-induced ventricular tachyarrhythmias. Intact and paraplegic (6-9 wk posttransection, T(5) spinal cord transection) rats were instrumented with a radiotelemetry device for recording arterial pressure, temperature, and ECG, and a snare was placed around the left main coronary artery. Following recovery, the susceptibility to ventricular arrhythmias (coronary artery occlusion) was determined in intact and paraplegic rats. In additional groups of matched intact and paraplegic rats, cardiac nerve growth factor content (ELISA) and cardiac sympathetic tonus were determined. Paraplegia, compared with intact, increased cardiac nerve growth factor content (2,146 +/- 286 vs. 180 +/- 36 pg/ml, P < 0.05) and cardiac sympathetic tonus (154 +/- 4 vs. 68 +/- 4 beats/min, P < 0.05) and decreased the ventricular arrhythmia threshold (3.6 +/- 0.2 vs. 4.9 +/- 0.2 min, P < 0.05). Thus altered autonomic behavior increases the susceptibility to ventricular arrhythmias in paraplegic rats.
authors.affiliation: Department of Physiology, Wayne State Univ. School of Medicine, 540 E. Canfield Ave., Detroit, MI 48201, USA.
authors.forename: Heidi L
authors.initials: HL
authors.lastname: Lujan
authors.forename: Ying
authors.initials: Y
authors.lastname: Chen
authors.forename: Stephen E
authors.initials: SE
authors.lastname: Dicarlo
mesh_terms: D058671:Adrenergic beta-1 Receptor Antagonists; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure; D001831:Body Temperature; D003243:Consciousness; D004195:Disease Models, Animal; D006321:Heart / Q000294:innervation*; D006339:Heart Rate; D008297:Male; D017202:Myocardial Ischemia / Q000150:complications* / Q000378:metabolism / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism*; D020932:Nerve Growth Factor / Q000378:metabolism*; D010264:Paraplegia / Q000150:complications* / Q000378:metabolism / Q000503:physiopathology; D010275:Parasympathetic Nervous System / Q000503:physiopathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D018342:Receptors, Adrenergic, beta-1 / Q000378:metabolism; D013119:Spinal Cord Injuries / Q000150:complications* / Q000378:metabolism / Q000503:physiopathology; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D017180:Tachycardia, Ventricular / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology; D015854:Up-Regulation
chemical_list: D058671:Adrenergic beta-1 Receptor Antagonists; D000319:Adrenergic beta-Antagonists; D018342:Receptors, Adrenergic, beta-1; D020932:Nerve Growth Factor