title: Streptomycin inhibits electrophysiological changes induced by stretching of chronically infarcted rat hearts.
abstract: OBJECTIVE
  To investigate stretch-induced electrophysiological changes in chronically infarcted hearts and the effect of streptomycin (SM) on these changes in vivo.
  
  
  METHODS
  Sixty Wistar rats were divided randomly into four groups: a control group (n=15), an SM group (n=15), a myocardial infarction (MI) group (n=15), and an MI+SM group (n=15). Chronic MI was obtained by ligating the left anterior descending branch (LAD) of rat hearts for eight weeks. The in vivo blockade of stretch-activated ion channels (SACs) was achieved by intramuscular injection of SM (180 mg/(kg∙d)) for seven days after operation. The hearts were stretched for 5 s by occlusion of the aortic arch. Suction electrodes were placed on the anterior wall of left ventricle to record the monophasic action potential (MAP). The effect of stretching was examined by assessing the 90% monophasic action potential duration (MAPD90), premature ventricular beats (PVBs), and ventricular tachycardia (VT).
  
  
  RESULTS
  The MAPD90 decreased during stretching in both the control (from (50.27±5.61) ms to (46.27±4.51) ms, P<0.05) and MI groups (from (65.47±6.38) ms to (57.47±5.76 ms), P<0.01). SM inhibited the decrease in MAPD90 during inflation ((46.27±4.51) ms vs. (49.53±3.52) ms, P<0.05 in normal hearts; (57.47±5.76) ms vs. (61.87±5.33) ms, P<0.05 in MI hearts). The occurrence of PVBs and VT in the MI group increased compared with that in the control group (PVB: 7.93±1.66 vs. 1.80±0.86, P<0.01; VT: 7 vs. 1, P<0.05). SM decreased the occurrence of PVBs in both normal and MI hearts (0.93±0.59 vs. 1.80±0.86 in normal hearts, P<0.05; 5.40±1.18 vs. 7.93±1.66 in MI hearts, P<0.01).
  
  
  CONCLUSIONS
  Stretch-induced MAPD90 changes and arrhythmias were observed in chronically infarcted myocardium. The use of SM in vivo decreased the incidence of PVBs but not of VT. This suggests that SACs may be involved in mechanoelectric feedback (MEF), but that there might be other mechanisms involved in causing VT in chronic MI.
authors.affiliation: Department of Cardiology, the First Affiliated Hospital of Harbin Medical University, Harbin 150001, China; Department of Chinese Medicine, Women's Hospital, School of Medicine, Zhejiang University, Hangzhou 310006, China.
authors.forename: Jun-xian
authors.initials: JX
authors.lastname: Cao
authors.forename: Lu
authors.initials: L
authors.lastname: Fu
authors.forename: Qian-ping
authors.initials: QP
authors.lastname: Gao
authors.forename: Rong-sheng
authors.initials: RS
authors.lastname: Xie
authors.forename: Fan
authors.initials: F
authors.lastname: Qu
mesh_terms: D000200:Action Potentials / Q000187:drug effects*; D000818:Animals; D006329:Heart Conduction System / Q000187:drug effects / Q000503:physiopathology*; D015640:Ion Channel Gating / Q000187:drug effects*; D008297:Male; D040542:Mechanotransduction, Cellular / Q000187:drug effects*; D009203:Myocardial Infarction / Q000150:complications / Q000503:physiopathology*; D051381:Rats; D017208:Rats, Wistar; D013307:Streptomycin / Q000494:pharmacology*; D013314:Stress, Mechanical; D017180:Tachycardia, Ventricular / Q000209:etiology / Q000503:physiopathology*
chemical_list: D013307:Streptomycin
keywords: Arrhythmia; Mechanoelectric feedback; Monophasic action potential; Myocardial infarction; Streptomycin