The Role of Myocardial Gap Junction in Ischemia-Reperfusion Injury in Senescent Rabbit Myocardium.
10.4326/jjcvs.30.165
- VernacularTitle:加齢が心筋虚血耐性とｉｓｃｈｅｍｉｃ ｐｒｅｃｏｎｄｉｔｉｏｎｉｎｇに及ぼす影響 ｇａｐ結合の関与について
- Author:
Yasunari Nakai
;
Hitoshi Horimoto
;
Hiroaki Shimomura
;
Tetsuya Hayashi
;
Yasushi Kitaura
;
Keiichiro Kondo
;
Kunio Asada
;
Shinjiro Sasaki
- Publication Type:Journal Article
- Keywords:
ischemic preconditioning
- From:Japanese Journal of Cardiovascular Surgery
2001;30(4):165-170
- CountryJapan
- Language:Japanese
-
Abstract:
Objective. We investigated whether the aging-related decrease in gap junction expression affects myocardial response against ischemia-reperfusion injury of the rabbit myocardium. Methods. Isolated aged (≥135 weeks) or mature (15-20 weeks) rabbit hearts were perfused with Krebs-Henseleit solution via a Langendorff apparatus, and were divided into five groups as follows: 7 mature hearts served as mature controls (Group A), 7 mature hearts underwent ischemic preconditioning (IPC) consisting of two cycles of global ischemia for 5min followed by reperfusion for 5min (Group B), 7 aged hearts served as aged control (Group C), 7 aged hearts underwent IPC (Group D) and 7 mature hearts received 1mM of gap junction uncoupler heptanol for 5min (Group E). Then, all hearts were subjected to 1h of left anterior descending coronary artery occlusion followed by 1h of reperfusion. Left ventricular pressure, ischemic zone monophasic action potential and coronary flow were measured throughout the experiment and the infarct size (IS) was determined at the end of the experiment. Gap junction expression was investigated by the electron microscopy. Results. The IS of Group A was 39.1±3.8 (%) and that of Group B was 26.9±3.8 (%)* (*p<0.05 vs. Group A). The IS of Group C was 19.3± 1.6(%)*. That of Group D was 43.6±5.8 (%)# (#p<0.05 vs. Group C). IS of Group E was 24.3±1.6 (%)*. Electron microscopic findings demonstrated that gap junction expression in aged hearts was less prominent than in mature ones. Conclusion. These data suggested that aged myocardium might be more tolerant of ischemic insult than that of mature heart, and that the mechanism might be related to the aging-related change of gap junction expression.
