title: Effect of physiologic ischemic training on protection of myocardial infarction in rabbits.
abstract: OBJECTIVE
  The aim of this study was to investigate the protective effect of physiologic ischemic training of normal skeletal muscle against myocardial infarction.
  
  
  METHODS
  Thirty-five rabbits were implanted with water balloon constrictors in the left ventricular branch to cause myocardial ischemia and an electrode near the left sciatic nerve for electric muscle stimulation for physiologic ischemic training. Three groups were randomly selected: the pure ischemia (PI) group received myocardial ischemia for 2 mins, two times a day, five times a week; the exercise training (ET) group received myocardial ischemia as did the PI group, plus 4 mins of physiologic ischemic training, two times a day, five times a week; and the sham-operated (SO) group was the sedentary controls. After 4 wks of training, the left ventricular branch was occluded to cause infarction. Infarct size was measured by magnetic resonance imaging; left ventricular ejection fraction, by echocardiogram; capillary density, by immunohistochemistry; and collateral circulation blood flow, by a microsphere technique.
  
  
  RESULTS
  The ET group's infarct size was significantly smaller than that of the PI group (P < 0.01) and the SO group (P < 0.01). Change in left ventricular ejection fraction in the ET group was significantly lower than in the SO group (P < 0.01), and capillary density in the ET group was significantly higher than in the PI group (P< 0.01) and the SO group (P < 0.01). Collateral circulation blood flow in the ET group was significantly higher than in the PI group (P < 0.01) and the SO group (P< 0.01). Capillary density was significantly correlated with endpoint collateral circulation blood flow (r = 0.91, P = 0.000), infarct size (r = -0.91, P = 0.000), and change in left ventricular ejection fraction (r = -0.94, P = 0.000).
  
  
  CONCLUSIONS
  Physiologic ischemic training of skeletal muscle may induce collateral circulation development in the myocardium, thus decreasing infarct size when infarction occurs.
authors.affiliation: Department of Rehabilitation Medicine, The First Affiliated Hospital of Nanjing Medical University, China.
authors.forename: Aicui
authors.initials: A
authors.lastname: Lin
authors.forename: Jianan
authors.initials: J
authors.lastname: Li
authors.forename: Yan
authors.initials: Y
authors.lastname: Zhao
authors.forename: Mingyue
authors.initials: M
authors.lastname: Xiao
authors.forename: Bo
authors.initials: B
authors.lastname: Xiao
authors.forename: Xiao
authors.initials: X
authors.lastname: Lu
authors.forename: Chunxiao
authors.initials: C
authors.lastname: Wan
mesh_terms: D000818:Animals; D002196:Capillaries / Q000473:pathology; D003097:Collateral Circulation; D007150:Immunohistochemistry; D019194:Ischemic Preconditioning; D008279:Magnetic Resonance Imaging; D008297:Male; D008853:Microscopy; D023421:Models, Animal; D018482:Muscle, Skeletal / Q000098:blood supply*; D009203:Myocardial Infarction / Q000473:pathology*; D015428:Myocardial Reperfusion Injury; D011817:Rabbits; D013318:Stroke Volume