title: A single five minute period of rapid atrial pacing fails to limit infarct size in the in situ rabbit heart.
abstract: OBJECTIVE
  Rapid pacing has been shown to precondition the dog heart against ischaemic dysrhythmia. The aim of this study was to determine whether rapid pacing could also limit infarct size.
  
  
  METHODS
  Rabbits (n = 5) were rapidly paced via the left atrium at 420-480 beats.min-1. Five min of rapid pacing and 10 min of recovery in sinus rhythm were followed by 45 min of regional ischaemia and 120 min of reperfusion. Control rabbits (n = 9) were treated identically without prior rapid pacing. Infarct size was determined in both groups using tetrazolium and expressed as a percentage of the area at risk demarcated by fluorescent microspheres. In a separate series of experiments, rapidly paced Langendorff perfused rabbit hearts (n = 9) were used to determine coronary flow under perfusion conditions designed to simulate the in vivo situation during rapid pacing.
  
  
  RESULTS
  Rapid pacing caused a fall in systolic pressure from 91.4(SEM 4.5) to 47.0(5.9) mm Hg (p < 0.01) and diastolic pressure from 67.2(2.9) to 23.6(3.2) mm Hg (p < 0.01). Both recovered within 30 s of cessation of pacing. During rapid pacing the action potential duration shortened from 192(13) to 128(5) ms (p = 0.01) and developed electrical alternans (n = 4). Following rapid pacing the ECG showed either ST depression or T wave inversion (n = 4). Despite these profound changes, rapid pacing did not reduce infarct size v control [52.7(4.6)% v 60.8(9.1)% of the area at risk, respectively]. The in vitro experiments estimated that rapid pacing would result in a reduction in coronary flow to 44% of that in sinus rhythm without a significant rise in lactate efflux.
  
  
  CONCLUSIONS
  In our model, pretreatment with rapid pacing fails to reduce infarct size. The most likely reason for this is that rapid pacing at a rate of 480 beats.min-1 does not cause myocardial ischaemia of sufficient severity to trigger the preconditioning response.
authors.affiliation: Hatter Institute for Cardiovascular Studies, Division of Cardiology, University College Hospital, London, United Kingdom.
authors.forename: M S
authors.initials: MS
authors.lastname: Marber
authors.forename: D M
authors.initials: DM
authors.lastname: Walker
authors.forename: D J
authors.initials: DJ
authors.lastname: Eveson
authors.forename: J M
authors.initials: JM
authors.lastname: Walker
authors.forename: D M
authors.initials: DM
authors.lastname: Yellon
mesh_terms: D000200:Action Potentials / Q000502:physiology; D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D002304:Cardiac Pacing, Artificial; D006321:Heart / Q000503:physiopathology; D008297:Male; D009203:Myocardial Infarction / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D015428:Myocardial Reperfusion Injury / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D009206:Myocardium / Q000473:pathology; D011817:Rabbits; D013997:Time Factors