ALTERED ELECTRICAL AND METABOLIC RESPONSE OF REPERFUSED MYOCARDIUM TOISCHEMIA AFTER RECOVERY FROM PRECEDING ISCHEMIA - EVIDENCE FOR ISCHEMIA SENSITIZED MYOCARDIUM

Citation
A. Nakagomi et al., ALTERED ELECTRICAL AND METABOLIC RESPONSE OF REPERFUSED MYOCARDIUM TOISCHEMIA AFTER RECOVERY FROM PRECEDING ISCHEMIA - EVIDENCE FOR ISCHEMIA SENSITIZED MYOCARDIUM, Cardiovascular Research, 27(4), 1993, pp. 571-577
Citations number
43
Categorie Soggetti
Cardiac & Cardiovascular System
Journal title
ISSN journal
00086363
Volume
27
Issue
4
Year of publication
1993
Pages
571 - 577
Database
ISI
SICI code
0008-6363(1993)27:4<571:AEAMRO>2.0.ZU;2-F
Abstract
Objective: The aim was to examine electrical and metabolic responses o f myocardium to ischaemia after recovery from preceding ischaemia. Met hods: In 23 open chest dogs (5 min occlusion group), the left anterior descending coronary artery was occluded three times in the following order: 2 min occlusion (Trial 1) followed by 15 min reperfusion; then 5 min occlusion followed by 90 min reperfusion and 2 min occlusion (Tr ial 2). In 15 control dogs, the 2 min occlusion was performed twice at a 110 min reperfusion interval; the former occlusion was also referre d to as Trial 1 and the latter as Trial 2. The dogs were monitored by epicardial surface ECG, while regional myocardial function was estimat ed by sonomicrometry. Continuous measurements of myocardial tissue PCO 2, pH, and extracellular K+ concentration were made concurrently. Resu lts: Both trial occlusions produced a biphasic change in R wave amplit ude characterised by a transient initial decrease succeeded by an incr ease with ST elevation. This biphasic change in R wave amplitude was i ndistinguishable between Trial 1 and Trial 2 in the control group. By contrast, in the 5 min group, the R wave amplitude initially decreased to a greater degree in Trial 2 than in Trial 1. More rapid contractil e failure was also noticed in Trial 2, suggesting the possible involve ment of mechanically induced electrical changes in the genesis of decr eased R wave amplitude. After 45-60 s of occlusion, however, the R wav e amplitude increased to a level much beyond the initial amplitude in Trial 1 [124.9(SEM 8.4)% at 120 s], whereas this level of increase was not observed in Trial 2 [106.5(7.8)%, p<0.05 v Trial 1]. There was al so reduced elevation of the ST segment in Trial 2: 3.6(0.8) mV v 6.5(0 .8) mV in Trial 1 at 120 s (p<0.05). This reduction in ST elevation wa s concomitant with decreased changes in PCO2, pH, and extracellular K concentration in Trial 2. These reduced changes in the ST segment and the metabolic variables were absent in the control group. Conclusions : These altered electrical responses of the myocardium may be the resu lt of more rapid early contractile failure and attenuated metabolic ch anges during ischaemia occurring after recovery from preceding ischaem ia.