title: [Metal stress-induced arrhythmia and thoracic spinal cord 1-5 nerve remodeling and myocardial electrophysiological remodeling in rats].
abstract: OBJECTIVE
  The study aimed to investigate the relationship between arrhythmia occurrence and nerve remodeling of thoracic spinal cord 1-5 nerves as well as myocardial electrophysiological remodeling in a metal stress rat model.
  
  
  METHODS
  Thirty SD rats (weight 180-250 g) were randomly divided into control group (n = 10), stress group (n = 10) and fluoxetine group (n = 10, 10 mg/kg i.p. for 3 weeks). Stress model (given by unpredicted chronic mild stress) was established according to Cronli's protocol. Following parameters were observed:(1) ECG waveform change and arrhythmias;(2) tissue field action potential duration (FAPD) of thoracic spinal cord 1-5 and cardiac tissue mapped by microelectrode arrays (MEA) technique;(3) myocardial growth-associated protein (GAP-43), tyrosine hydroxylase (TH), choline acetyltransferase (CHAT) distribution observed by immunofluorescence and confocal laser scanning microscope (LSCM).
  
  
  RESULTS
  Three weeks later: (1) The body weight, food intake, consumption of sugar water, the horizontal and vertical movement score, cleaning action of rats were significantly decreased, and fecal grains significantly increased, P-wave, P-R interval, QRS-wave and Q-T interval were significantly prolonged and heart rate was significantly reduced in stress group compared with control group (all P < 0.05). Incidence of ventricular premature beat was 80% in stress group and 0% in control group (P < 0.05). The FAPD of thoracic spinal cord 1-5 nerves [(144.25 ± 12.63)ms vs (79.56 ± 8.01)ms] and of cardiac tissue [LA(122.43 ± 19.34)ms vs (92.59 ± 7.61)ms, RA(149.89 ± 14.68)ms vs (105.18 ± 15.94)ms, LV(162.62 ± 7.04)ms vs (110.45 ± 6.92)ms, RV(152.21 ± 30.49)ms vs (131.06 ± 12.04)ms] were significantly prolonged, FAPD dispersion (FAPDd) significantly increased [thoracic spinal cord 1-5(13.3 ± 9.11)ms vs (9.36 ± 7.01)ms] in stress group compared with the control group. Disarrangement of myocardial cells, proliferation of collagen fiber, infiltration of neutrophil and lymphocytes in the cardiac tissue were also observed and distribution of GAP-43, TH and CHAT was significantly increased in stress group. (2) All these changes could be partly reversed by the treatment with fluoxetine.
  
  
  CONCLUSIONS
  Metal stress induced cardiac autonomic nerve and myocardial electrophysiological remodeling and ventricular arrhythmia in rats which could be significantly attenuated by fluoxetine in this model.
authors.affiliation: Department of Cardiology, Zhongshan Hospital Fudan University, Shanghai 200032, China.
authors.forename: Jia-Lu
authors.initials: JL
authors.lastname: Hu
authors.forename: Qi-Na
authors.initials: QN
authors.lastname: Zhou
authors.forename: Shang-Lei
authors.initials: SL
authors.lastname: Yang
authors.forename: Hua
authors.initials: H
authors.lastname: Chen
authors.forename: Ling
authors.initials: L
authors.lastname: Zhang
authors.forename: Yan
authors.initials: Y
authors.lastname: Yan
authors.forename: Yue-Mei
authors.initials: YM
authors.lastname: Hou
mesh_terms: D000818:Animals; D001145:Arrhythmias, Cardiac / Q000209:etiology / Q000503:physiopathology*; D002795:Choline O-Acetyltransferase / Q000378:metabolism; D005473:Fluoxetine / Q000627:therapeutic use; D019922:GAP-43 Protein / Q000378:metabolism; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D013116:Spinal Cord / Q000503:physiopathology; D013315:Stress, Psychological / Q000150:complications / Q000503:physiopathology*; D013900:Thoracic Nerves / Q000503:physiopathology*; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism; D020257:Ventricular Remodeling
chemical_list: D019922:GAP-43 Protein; D005473:Fluoxetine; D014446:Tyrosine 3-Monooxygenase; D002795:Choline O-Acetyltransferase