title: Electrophysiological characteristics of repetitive ischemic preconditioning in the pig heart.
abstract: S-T segment changes have been cited as evidence for preconditioning in the human heart during repeated angioplasty inflations. Opening of preformed collaterals, however, could explain these observations. We have measured the profile of S-T segment and monophasic action potential (MAP) changes in a species with low collateralization. Open-chested pigs were subjected to two cycles of 8-min LAD occlusion and 8-min reperfusion prior to 60-min ischemia and 2-h reperfusion. Two epicardial ECGs and MAP were continuously recorded from the ischemic zone and one ECG from the normal zone. Flow was measured using Xenon washout. Infarct (IS) and risk zone (RZ) sizes were assessed after reperfusion in a subset of six pigs and confirmed profound protection with preconditioning (IS/RZ = 14 +/- 9% v 42 +/- 3% in controls, P < 0.05). S-T segment elevation was smaller early in the 2nd or 3rd (0-3 min) ischemic cycles than in the 1st. In contrast, in the 1st ischemic cycle, MAP duration after 3 min was reduced to 90 +/- 2% control and this was further reduced in the 2nd and 3rd ischemic episodes to 74 +/- 4% and 77 +/- 3% respectively. Thus, preconditioning increased APD shortening while simultaneously decreasing S-T segment elevation during the early minutes of ischemia. It therefore seems unlikely that the ability of preconditioning to limit S-T segment changes is related to limitations in APD shortening. All electrophysiological differences were lost later during ischemia. Collateral flow during the three ischemic cycles was 4.8 +/- 3.7, 5.8 +/- 2.3 and 5.6 +/- 2.9% (n = 5/grp, ns) respectively. Thus, in the absence of a significant increase in collateral flow. S-T segment and MAP changes provide an index of preconditioning but only during the first few minutes of occlusion. S-T segment changes observed during PTCA may therefore reflect genuine preconditioning in man although the contribution of ischemia-induced increases in collateral flow cannot be ignored.
authors.affiliation: Rayne Institute, St Thomas' Hospital, London, UK.
authors.forename: M J
authors.initials: MJ
authors.lastname: Shattock
authors.forename: C S
authors.initials: CS
authors.lastname: Lawson
authors.forename: D J
authors.initials: DJ
authors.lastname: Hearse
authors.forename: J M
authors.initials: JM
authors.lastname: Downey
mesh_terms: D000200:Action Potentials; D000818:Animals; D003097:Collateral Circulation; D003331:Coronary Vessels / Q000502:physiology*; D004562:Electrocardiography; D004594:Electrophysiology / Q000379:methods; D006321:Heart / Q000502:physiology*; D006801:Humans; D019194:Ischemic Preconditioning; D008297:Male; D015425:Myocardial Reperfusion; D013552:Swine; D013997:Time Factors