title: High spinal anesthesia does not alter experimental myocardial infarction size or ischemic preconditioning.
abstract: OBJECTIVE
  The role of the central nervous system in the development of myocardial infarction and ventricular fibrillation in virgin and ischemically preconditioned myocardium was investigated.
  
  
  METHODS
  Infarct size and ventricular arrhythmias were assessed after regional ischemia-reperfusion. Animals were randomly assigned to four groups: (1) preconditioned, central nervous system intact; (2) nonpreconditioned, nervous system intact; (3) preconditioned, nervous system blocked; and (4) nonpreconditioned, nervous system blocked. Differences in hemodynamics and infarct size were assessed with analysis of variance, and differences in ventricular fibrillation were assessed with the Kruskal-Wallis test.
  
  
  METHODS
  Experiments were performed in the Anesthesiology Research Laboratory at a medical center.
  
  
  METHODS
  Anesthetized open-chest New Zealand white rabbits were used for these studies.
  
  
  METHODS
  Rabbits underwent 30 minutes of coronary artery occlusion and 3 hours of reperfusion. The central nervous system was blocked with total spinal anesthesia. Ischemic preconditioning was elicited with 5 minutes of coronary artery occlusion and 10 minutes of reperfusion. Infarction was assessed with tetrazolium and expressed as a percentage of the risk zone (mean +/- SEM).
  
  
  RESULTS
  Preconditioning resulted in infarct size limitation compared with the control (8% +/- 4% v 43% +/- 5%; p < 0.001) and delayed the onset of fibrillation (15.5 minutes v 11 minutes; p = 0.001). Spinal blockade neither altered nonpreconditioned infarct size nor attenuated preconditioning (32% +/- 7% v 8% +/- 3%; p = 0.04), but it was associated with ventricular fibrillation in 24/25 rabbits as compared with 6/14 rabbits without blockade. In blocked animals, preconditioning resulted in a decreased duration of fibrillation (2.5 minutes v 12.5 minutes; p = 0.0004). However, spinal blockade eliminated the preconditioning-induced delay in fibrillation (10 minutes v 12 minutes; p = NS).
  
  
  CONCLUSIONS
  It is concluded that (1) activation of efferent sympathetic nerves is not necessary for ischemic preconditioning; (2) preconditioning delays the onset of ventricular arrhythmias; and (3) spinal blockade exacerbates ischemia-induced ventricular arrhythmias.
authors.affiliation: Department of Anesthesiology, Oregon Health Sciences University, Portland, USA.
authors.forename: R
authors.initials: R
authors.lastname: Haessler
authors.forename: R A
authors.initials: RA
authors.lastname: Wolff
authors.forename: G L
authors.initials: GL
authors.lastname: Chien
authors.forename: R F
authors.initials: RF
authors.lastname: Davis
authors.forename: D M
authors.initials: DM
authors.lastname: van Winkle
mesh_terms: D000775:Anesthesia, Spinal; D000818:Animals; D001794:Blood Pressure; D006339:Heart Rate; D009203:Myocardial Infarction / Q000503:physiopathology*; D009206:Myocardium / Q000473:pathology; D009407:Nerve Block; D009929:Organ Size; D011817:Rabbits; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D014693:Ventricular Fibrillation / Q000503:physiopathology