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. 2001 Mar;85(3):331–336. doi: 10.1136/heart.85.3.331

Exercise directly enhances myocardial tolerance to ischaemia-reperfusion injury in the rat through a protein kinase C mediated mechanism

N Yamashita 1, G Baxter 1, D Yellon 1
PMCID: PMC1729658  PMID: 11179278

Abstract

OBJECTIVE—To determine whether exercise is capable of protecting the myocardium from experimental infarction and to explore the involvement of protein kinase C, a key signalling protein, in the development of any protection observed.
METHODS—Rats were exercised on a treadmill for 30 minutes at 23-27 m/min. Sham treated animals were placed on the stationary treadmill but not exercised. Twenty four hours later, hearts were Langendorff perfused and subjected to 35 minute left main coronary artery occlusion followed by 120 minute reperfusion. Infarct size was determined by tetrazolium staining and expressed as a percentage of the risk zone (I/R%). To examine the potential signalling pathway, animals were treated with either the selective protein kinase C inhibitor chelerythrine, 5 mg/kg intraperitoneally, or with vehicle 10 minutes before the exercise or sham treadmill period.
RESULTS—In the non-exercised group, mean (SEM) I/R was 48.4 (3.0)%. In the exercised group, infarct size was reduced to 17.3 (3.0)% (p < 0.01). Infarct size limitation induced by exercise was abolished by chelerythrine (I/R 45.0 (6.0)%). Chelerythrine pretreatment alone did not have any effect on infarct size (I/R 51.1 (3.9)%). Differences in infarct size were independent of risk zone size and myocardial contractile function during ischaemia-reperfusion.
CONCLUSIONS—Experimental moderate exercise induces protection against myocardial infarction 24 hours later. Protein kinase C activation during exercise appears to be an important signal mediator of this protective response.


Keywords: exercise; myocardial infarction; cardioprotection; protein kinase C

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Figure 1  .

Figure 1  

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Experimental protocol. Rats were screened before the experiment for their ability to run on a treadmill. At least 10 days after screening, those animals that were able to run for 30 minutes were randomly assigned to either treadmill exercise or a corresponding sham period (day 1). Twenty four hours later (day 2), hearts were isolated and Langendorff perfused. They were subjected to 35 minutes of coronary artery occlusion and reperfusion, after which the infarct size was assessed. ip, intraperitoneally.

Figure 2  .

Figure 2  

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Changes in coronary flow during an in vitro (Langendorff perfusion) ischaemia-reperfusion protocol. Rats were treated with vehicle or chelerythrine chloride (5 mg/kg intraperitoneally) 10 minutes before exercise or sham treatment and 24 hours before ischaemia (see fig 1). *p < 0.05 v sham + vehicle group (n = 7/group).

Figure 3  .

Figure 3  

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(A) Risk zone size expressed as percentage of total left ventricle muscle volume. (B) Infarct size expressed as percentage infarction of the risk zone in hearts subjected to 35 minutes of coronary occlusion followed by 120 minutes of reperfusion. Values are means, error bars = SEM. Rats were treated with vehicle or chelerythrine chloride (5 mg/kg intraperitoneally) 10 minutes before exercise or sham treatment and 24 hours before ischaemia (see fig 1). *p < 0.01 v sham + vehicle group (n = 7/group).

Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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