{"id":{"repo_id":"ajou","oai_identifier":"oai:repository.ajou.ac.kr:201003/8626"},"canonical_url":"https://search.dev.ndltd.org/etd/ajou/oai:repository.ajou.ac.kr:201003/8626","repository":{"repo_id":"ajou","name":"Ajou University","base_url":"http://repository.ajou.ac.kr/oai/request"},"display":{"title":"Isoflurane-induced post-conditioning in senescent hearts is attenuated by failure to activate reperfusion injury salvage kinase pathway","abstract":"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.","abstract_html":"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.","abstract_has_math":false,"creators":["장, 동진"],"institution":null,"degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":["김, 진수","대학원 의학과","200924408"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2013,"date_issued":"2013-12-16T06:32:28Z","date_published":"2013-12-16T06:32:28Z","updated_at":"2026-07-24T00:51:42Z","subjects":["Heart","isoflurane","post-conditioning","RISK pathway","심근","후조건화"],"languages":["en"],"rights":[],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000013446","000000013446"],"render_values":[{"text":"http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000013446","href":"http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000013446","code":true},{"text":"000000013446","href":null,"code":true}]}]},"links":{"outbound_url":"http://repository.ajou.ac.kr/handle/201003/8626","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["김, 진수","대학원 의학과","200924408","장, 동진"]},{"key":"dc:creator","label":"Author","values":["장, 동진"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2013-12-16T06:32:28Z","2013"]},{"key":"dc:type","label":"Dc Type","values":["Thesis","Theses"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Heart","isoflurane","post-conditioning","RISK pathway","심근","후조건화"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["en"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["http://repository.ajou.ac.kr/handle/201003/8626","http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000013446","000000013446"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["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.","본 연구에서는 고령 쥐에서 isoflurane 을 심근의 재관류 시기에 투여하였을 때 흡입마취제의 심근보호 효과를 젊은 쥐와 비교하여 알아보고자 하였다. 또한 이러한 차이를 나타내는 이유로 reperfusion injury salvage kinase (RISK) pathway 의 활성화 정도를 측정하여 비교해 보고자 하였다. 수컷 Wistar 쥐를 나이에 따라 3-5 개월 된 젊은 쥐와 20-24 개월 된 고령 쥐로 나누고 각각을 다시 재관류 시작 3 분 전부터 2 분 후까지 5 분간 isoflurane (1최소 폐포 농도)을 투여 받는 그룹(ISO popstC 군)과 그렇지 않은 그룹(대조군)으로 무작위로 나누어 실험을 진행하였다. 모든 그룹에서 관상동맥의 결찰은 30 분간 유지하였고 이후 2 시간 동안 재관류를 하였다. 재관류 시작 후 15 분이 경과하였을 때 얻은 심근 조직으로 western blot analysis 를 시행하여 ERK1/2, Akt, GSK3β 의 인산화 정도를 측정하였다. 젊은 쥐에서는 isoflurane 을 투여한 군에서 심근 경색의 정도가 대조군에 비하여 감소하여 나타났으나 (ISO postC 군; 56±8% of left ventricle area at risk, 대조군; 68±4%, 평균±표준편차) 고령 쥐에서는 유의한 차이를 보이지 않았다 (ISO postC 군; 56±8%, 대조군; 56±10%). Isoflurane 의 투여 시 젋은 쥐에서는 ERK1/2, Akt, GSK3β 의 인산화 정도가 증가하였으나 고령 쥐에서는 차이가 없었다. Isoflurane 의 후조건화 효과가 젊은 쥐에서는 유의하게 나타났으나 고령 쥐에서는 나타나지 않았고 이것은 고령 쥐에서 RISK pathway 가 활성화 되지 못한 것과 연관이 있을 것으로 보인다.","ABSTRACT i TABLE OF CONTENTS ii LIST OF FIGURES iii LIST OF TABLES iv Ⅰ. INTRODUCTION 1 Ⅱ. MATERIALS AND METHODS 3 Ⅲ. RESULTS 7 Ⅳ. DISCUSSION 13 Ⅴ. CONCLUSION 16 REFERENCES 17 국문요약 21 Fig.1. Schematic diagram depicting the experimental protocol 4 Fig.2. Myocardial infarct size 9 Fig.3. Western blot analysis 10 Table 1. Hemodynamic data 7 Table 2. Weights and area at risk 8","Doctor"]},{"key":"dc:title","label":"Title","values":["Isoflurane-induced post-conditioning in senescent hearts is attenuated by failure to activate reperfusion injury salvage kinase pathway","노화된 심근에서 isoflurane 후조건화의 보호효과 감소에 대한 연구: Reperfusion Injury Salvage Kinase 활성화의 역할"]}]}],"canonical_facts":{"dc:contributor":["김, 진수","대학원 의학과","200924408","장, 동진"],"dc:creator":["장, 동진"],"dc:date":["2013-12-16T06:32:28Z","2013"],"dc:description":["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.","본 연구에서는 고령 쥐에서 isoflurane 을 심근의 재관류 시기에 투여하였을 때 흡입마취제의 심근보호 효과를 젊은 쥐와 비교하여 알아보고자 하였다. 또한 이러한 차이를 나타내는 이유로 reperfusion injury salvage kinase (RISK) pathway 의 활성화 정도를 측정하여 비교해 보고자 하였다. 수컷 Wistar 쥐를 나이에 따라 3-5 개월 된 젊은 쥐와 20-24 개월 된 고령 쥐로 나누고 각각을 다시 재관류 시작 3 분 전부터 2 분 후까지 5 분간 isoflurane (1최소 폐포 농도)을 투여 받는 그룹(ISO popstC 군)과 그렇지 않은 그룹(대조군)으로 무작위로 나누어 실험을 진행하였다. 모든 그룹에서 관상동맥의 결찰은 30 분간 유지하였고 이후 2 시간 동안 재관류를 하였다. 재관류 시작 후 15 분이 경과하였을 때 얻은 심근 조직으로 western blot analysis 를 시행하여 ERK1/2, Akt, GSK3β 의 인산화 정도를 측정하였다. 젊은 쥐에서는 isoflurane 을 투여한 군에서 심근 경색의 정도가 대조군에 비하여 감소하여 나타났으나 (ISO postC 군; 56±8% of left ventricle area at risk, 대조군; 68±4%, 평균±표준편차) 고령 쥐에서는 유의한 차이를 보이지 않았다 (ISO postC 군; 56±8%, 대조군; 56±10%). Isoflurane 의 투여 시 젋은 쥐에서는 ERK1/2, Akt, GSK3β 의 인산화 정도가 증가하였으나 고령 쥐에서는 차이가 없었다. Isoflurane 의 후조건화 효과가 젊은 쥐에서는 유의하게 나타났으나 고령 쥐에서는 나타나지 않았고 이것은 고령 쥐에서 RISK pathway 가 활성화 되지 못한 것과 연관이 있을 것으로 보인다.","ABSTRACT i TABLE OF CONTENTS ii LIST OF FIGURES iii LIST OF TABLES iv Ⅰ. INTRODUCTION 1 Ⅱ. MATERIALS AND METHODS 3 Ⅲ. RESULTS 7 Ⅳ. DISCUSSION 13 Ⅴ. CONCLUSION 16 REFERENCES 17 국문요약 21 Fig.1. Schematic diagram depicting the experimental protocol 4 Fig.2. Myocardial infarct size 9 Fig.3. Western blot analysis 10 Table 1. Hemodynamic data 7 Table 2. Weights and area at risk 8","Doctor"],"dc:identifier":["http://repository.ajou.ac.kr/handle/201003/8626","http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000013446","000000013446"],"dc:language":["en"],"dc:subject":["Heart","isoflurane","post-conditioning","RISK pathway","심근","후조건화"],"dc:title":["Isoflurane-induced post-conditioning in senescent hearts is attenuated by failure to activate reperfusion injury salvage kinase pathway","노화된 심근에서 isoflurane 후조건화의 보호효과 감소에 대한 연구: Reperfusion Injury Salvage Kinase 활성화의 역할"],"dc:type":["Thesis","Theses"]},"updated_at":"2026-07-24T00:51:42Z"}