Myocardial glycogen depletion cannot explain the cardioprotective effects of ischemic preconditioning in the rat heart

Gregory K. Asimakis

Research output: Contribution to journalArticlepeer-review

22 Scopus citations


The mechanism of ischemic preconditioning remains unknown. The role of glycogen depletion prior to prolonged ischemia was examined as a potential mechanism of ischemic preconditioning. The glycogen content of the rat heart varies in a 24-h rhythm. In a retrospective study, the relationships between the time of day the animals were sacrificed, pre-ischemic myocardial glycogen content, and post-ischemic functional recovery were assessed in non-conditioned and ischemically preconditioned hearts. The analyses were performed on previously published data . After an equilibration perfusion, isolated rat hearts were given 40 min of global ischemia followed by 30 min of reperfusion. Preconditioned hearts received 5 min of ischemia followed by a 5-min recovery period prior to the 40-min ischemic period. Some of the hearts were freeze-clamped immediately prior to the 40 min ischemic period to determine pre-ischemic glycogen content. Pre-ischemic glycogen was higher in the morning than afternoon. The time of day correlated significantly with the pre-ischemic glycogen content of non-conditioned (r = 0.67; P < 0.005) and preconditioned (r = 0.79; P < 0.001) hearts. However, time of day did not correlate significantly with post-ischemic recovery of heart rate x developed pressure (HR x DP) or end-diastolic pressure (EDP) in either the non-conditioned or preconditioned hearts. The relationships were also assessed by subdividing the groups into either morning (a.m.) or afternoon (p.m.) hearts. The pre-ischemic glycogen content was lower in the non-conditioned-p.m. (n = 5) hearts compared to the non-conditioned-a.m. (n = 10) hearts (67.6 ± 9.0 v 128.1 ± 13.3 nmol glucose/mg protein, P < 0.005). However, there were no significant differences between p.m. (n = 13) and a.m. (n = 9) non-conditioned hearts with respect to post-ischemic recovery of HR x DP (20.6 ± 4 v 12.0 ± 4% of baseline, respectively, P = N.S.). In contrast, preconditioned-p.m. (n = 6) and -a.m. (n = 7) had pre-ischemic glycogen contents of 49.6 ± 6 and 76.6 ± 5.0 nmol glucose/mg protein, respectively. These glycogen values were not significantly different from the non-conditioned-p.m. hearts (67.6 nmol/mg protein). However, post-ischemic recovery of HR x DP in the preconditioned-p.m. (n = 5) and -a.m. (n = 6) hearts were 54.6 ± 5 and 51.4 ± 8% of baseline, respectively (these values were significantly higher (P < 0.05) than the recovery for the non-conditioned-p.m. and -a.m. hearts). The results imply that the cardioprotection of ischemic preconditioning cannot be explained solely by myocardial glycogen depletion.

Original languageEnglish (US)
Pages (from-to)563-570
Number of pages8
JournalJournal of Molecular and Cellular Cardiology
Issue number3
StatePublished - Mar 1996
Externally publishedYes


  • Ischemic injury
  • Ischemic preconditioning
  • Myocardial glycogen
  • Rat heart

ASJC Scopus subject areas

  • Molecular Biology
  • Cardiology and Cardiovascular Medicine


Dive into the research topics of 'Myocardial glycogen depletion cannot explain the cardioprotective effects of ischemic preconditioning in the rat heart'. Together they form a unique fingerprint.

Cite this