Mj. Shattock et al., ELECTROPHYSIOLOGICAL CHARACTERISTICS OF REPETITIVE ISCHEMIC PRECONDITIONING IN THE PIG-HEART, Journal of Molecular and Cellular Cardiology, 28(6), 1996, pp. 1339-1347
S-T segment changes have been cited as evidence for preconditioning in
the human heart during repeated angioplasty inflations. Opening of pr
eformed collaterals, however, could explain these observations. We hav
e measured the profile of S-T segment and monophasic action potential
(MAP) changes in a species with low collateralization. Open-chested pi
gs were subjected to two cycles of 8-min LAD occlusion and 8-min reper
fusion prior to 60-min ischemia and 2-h reperfusion. Two epicardial EC
Gs and MAP were continuously recorded from the ischemic zone and one E
CG from the normal zone. Flow was measured using Xenon washout. Infarc
t (IS) and risk zone (RZ) sizes were assessed after reperfusion in a s
ubset of six pigs and confirmed profound protection with preconditioni
ng (IS/RZ = 14 +/- 9% v 42 +/- 3% in controls, P<0.05). S-T segment el
evation 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 redu
ced in the 2nd and 3rd ischemic episodes to 74 +/- 4% and 77 +/- 3% re
spectively. Thus, preconditioning increased APD shortening while simul
taneously decreasing S-T segment elevation during the early minutes of
ischemia. It therefore seems unlikely that the ability of preconditio
ning to limit S-T segment changes is related to limitations in APD sho
rtening. All electrophysiological differences were lost later during i
schemia. 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 segme
nt and MAP changes provide an index of preconditioning but only during
the first few minutes of occlusion. S-T segment changes observed duri
ng PTCA may therefore reflect genuine preconditioning in man although
the contribution of ischemia-induced increases in collateral flow cann
ot be ignored. (C) 1996 Academic Press Limited