Isoflurane-induced post-conditioning in senescent hearts is attenuated by failure to activate reperfusion injury salvage kinase pathway

BACKGROUND: We investigated the cardioprotective effects of isoflurane administered at the onset of reperfusion in senescent rat in vivo, and the activation of the reperfusion injury salvage kinase (RISK) pathway to address a possible mechanism underlying age-related differences. METHODS AND RESULTS: Male Wistar rats were assigned to age groups (young, 3–5 months; old, 20–24 months), and randomly selected to receive isoflurane (1 minimum alveolar concentration) or not for 3 min before and 2 min after reperfusion (ISO postC). Rats were subjected to coronary occlusion for 30 min followed by 2 h of reperfusion. Western blot analysis was used to assess the phosphorylation of extracellular signal-regulated kinase (ERK1/2), Akt, and GSK3β 15 min after reperfusion. Brief administration of isoflurane 3min before and 2 min after the initiation of early reperfusion reducedinfarct size (56 ± 8% of left ventricular area at risk, mean ± standard deviation) compared with controls (68 ± 4%) in young rats, but had no effect in old rats (56 ± 8% in ISO postC and 56 ± 10% in control, respectively). Phosphorylation of ERK1/2, Akt, and GSK3β were increased in the young ISO postC group but not in the old ISO postC group compared with control groups of the respective ages. CONCLUSIONS: We demonstrated that isoflurane postconditions the heart in young but not in senescent rats. Failure to activate RISK pathway may contribute to attenuation of isofluraneinduced post-conditioning effect in senescent rats.

Author dc:creator

• 장, 동진

Contributors dc:contributor

• 김, 진수
• 대학원 의학과
• 200924408

• Heart
• isoflurane
• post-conditioning
• RISK pathway
• 심근
• 후조건화

Language dc:language

en

Identifier

http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000013446
000000013446

OAI identifier oai:identifier

oai:repository.ajou.ac.kr:201003/8626