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Isoflurane‐induced post‐conditioning in senescent hearts is attenuated by failure to activate reperfusion injury salvage kinase pathway
Author(s) -
CHANG D. J.,
CHANG C. H.,
KIM J. S.,
HONG Y. W.,
LEE W. K.,
SHIM Y. H.
Publication year - 2012
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1111/j.1399-6576.2012.02702.x
Subject(s) - isoflurane , medicine , protein kinase b , kinase , coronary occlusion , anesthesia , reperfusion injury , phosphorylation , endocrinology , myocardial infarction , pharmacology , cardiology , ischemia , biochemistry , biology
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 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 post C ). 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 ( ERK 1/2), A kt, and GSK 3β 15 min after reperfusion. Results Brief administration of isoflurane 3 min before and 2 min after the initiation of early reperfusion reduced infarct 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 post C and 56 ± 10% in control, respectively). Phosphorylation of ERK 1/2, A kt, and GSK 3β were increased in the young ISO post C group but not in the old ISO postC group compared with control groups of the respective ages. Conclusions We demonstrated that isoflurane post‐conditions the heart in young but not in senescent rats. Failure to activate RISK pathway may contribute to attenuation of isoflurane‐induced post‐conditioning effect in senescent rats.