ABSTRACT
Protective effect and mechanism of electroacupuncture (EA) on acute reperfusion ventricular arrhthmia was investigated. Ventricular arrhythmia was induced by occlusion of the proximal left anterior descend (LAD) branch of coronary artery for 5 min and followed with 15 min reperfusion . EA on acupoint "Neiguan", "Jianshi" was performed at 30 min before ligation and continued another 5 min during ischemia. Isoprenaline (20, 30 and 50 μg/kg) or atropine (1 mg/kg) was intravenously injected at 5min before ischemia. The results showed that EA significantly decreased the incidence of ischemia/reperfusion (I/R) induced ventricular tachycardia (VT), ventricular fibrillation (VF) and mortality as compared to I/R group. Atropine partially suppressed the EA's effect of antiarrhythmia; Isoprenaline increased the incidence and severity of reperfusion arrhythmia, which was inhibited by EA, but this inhibition of EA was blocked with increasing dose of isoprenaline. The results indicated that EA treatment could prevent the occurrence of reperfusion ventricular arrhythmia in rats with myocardial ischemia, and its mechanism might be related to the regulation of EA on the β-adrenoceptors and M-cholinergic receptor activation in myocardium.
ABSTRACT
Protective effect and mechanism of electroacupuncture (EA) on acute reperfusion ventricular arrhthmia was investigated. Ventricular arrhythmia was induced by occlusion of the proximal left anterior descend (LAD) branch of coronary artery for 5 min and followed with 15 min reperfusion. EA on acupoint "Neiguan", "Jianshi" was performed at 30 min before ligation and continued another 5 min during ischemia. Isoprenaline (20, 30 and 50 microg/kg) or atropine (1 mg/ kg) was intravenously injected at 5 min before ischemia. The results showed that EA significantly decreased the incidence of ischemia/reperfusion (I/R) induced ventricular tachycardia (VT), ventricular fibrillation (VF) and mortality as compared to I/R group. Atropine partially suppressed the EA's effect of antiarrhythmia; Isoprenaline increased the incidence and severity of reperfusion arrhythmia, which was inhibited by EA, but this inhibition of EA was blocked with increasing dose of isoprenaline. The results indicated that EA treatment could prevent the occurrence of reperfusion ventricular arrhythmia in rats with myocardial ischemia, and its mechanism might be related to the regulation of EA on the beta-adrenoceptors and M-cholinergic receptor activation in myocardium.
ABSTRACT
The effect of magnetic stimulation (MS) on sciatic nerve injury was observed. After sciatic nerve was crushed in 40 Sprague Dawley (SD) rats, one randomly selected group (group D) was subjected, from the 4th day post-operatively to 3 min of continuous 70% of maximum output of MS daily for 8 weeks. The other group (group E) served as a control group. The nerve regeneration and motor function recovery were evaluated by walking track analysis (sciatic function index, SFI; toe spreading reflex, TSR), electrophysiological, histological and acetylcholineesterase histochemistry. The SFI in the group D was greater than in the group E with the difference being statistically significant (P < 0.01). TSR reached its peak on the 4th day in the group D and on the 10th day in the group E respectively. The amplitude and velocity of MCAP and NCAP in the group D was greater than in the group E with the difference being statistically significant (P < 0.01), while the latency and duration of MCAP and NCAP in the group D were less than in the group E with the difference being also statistically significant (P < 0.01). Histological examination showed the mean axon count above the lesion for thick myelinated fibers (> 6.5 microns) in the group D was greater than in the control group with the difference being statistically significant (P < 0.01), while the mean axon count below the lesion for thick myelinated fibers was less than that in the group E with the difference being statistically significant (P < 0.01). The mean axon count above the lesion for thin myelinated fibers (2-6.5 microns) in the group D was greater than that in the group E with the difference being statistically significant (P < 0.05), while the mean axon count below the lesion for thin myelinated in the group D was greater than that in the group E with the difference being statistically significant (P < 0.01). Acetylcholine esterase examination showed that the MS could significantly increase the number of the motor neurons. There was no significant difference in the number of the motor neurons between the treatment side and the normal side (P > 0.05). It can be concluded that MS can enhance functional recovery and has a considerable effect in the treatment of the peripheral nerve injury.
Subject(s)
Animals , Rats , Acetylcholinesterase , Metabolism , Electromagnetic Phenomena , Motor Neurons , Physiology , Nerve Regeneration , Random Allocation , Rats, Sprague-Dawley , Sciatic Nerve , Wounds and Injuries , Sciatic Neuropathy , RehabilitationABSTRACT
The effect of magnetic stimulation (MS) on sciatic nerve injury was observed. After sciatic nerve was crushed in 40 Sprague Dawley (SD) rats, one randomly selected group (group D) was subjected, from the 4th day post-operatively to 3 min of continuous 70% of maximum output of MS daily for 8 weeks. The other group (group E) served as a control group. The nerve regeneration and motor function recovery were evaluated by walking track analysis (sciatic function index, SFI; toe spreading reflex, TSR), electrophysiological, histological and acetylcholineesterase histochemistry. The SFI in the group D was greater than in the group E with the difference being statistically significant (P 6.5 microns) in the group D was greater than in the control group with the difference being statistically significant (P 0.05). It can be concluded that MS can enhance functional recovery and has a considerable effect in the treatment of the peripheral nerve injury.