Expression of Heat Shock Protein After Ischemic Preconditioning in Rabbit Hearts

Abstract

Previous studies have shown that preconditioning (PC) with a brief ischemic episode induces heat shock protein (HSP) in cardiac tissue. However, it is unclear when and where in the left ventricle HSP is expressed after PC. Hence, the expression of HSP was studied in rabbit hearts at various time intervals after PC using immunohistochemical methods. Rabbits were preconditioned four times with 5 min of occlusion and 5 min of reperfusion of the coronary artery and then were killed at 0, 3, 24, 48, 72 and 168 h after the PC (n=4, for each time interval). Samples were obtained from the subendocardium and subepicardium of the preconditioned and nonpreconditioned wall and these were processed to 4 m thick cryosections. The sections were immunolabelled with mouse monoclonal IgGs against HSP 72/73. Positive immunoreactivity was observed as early as 3 h after PC, persisting up to 72 h but not detected at 168 h. HSP was expressed not only in the preconditioned myocardium but also in the remote nonpreconditioned myocardium. There was a wide variation in expression among myocytes. Expression was dominant in myocytes compared with vessel walls. It was concluded that PC induced transient and inhomogeneous expression of HSP in rabbit hearts. (Jpn Circ J 1998; 62: 512 -516)

Plasma levels of Hsp70 and anti-Hsp70 antibody predict risk of acute coronary syndrome

“…It is possible that the stress response is only transient or short term, not chronic and persistent state. Tanaka et al (Tanaka et al 1998) reported that expression of Hsp70 appeared within 3 h after ischemic stress, that it persisted for up to 72 h, and that it was not detected at 168 h in rabbit hearts. Based on this finding, we suggest that the sources of circulating Hsp70 after AMI may result from the damaged or necrosis of cardiomyocytes and severe endothelial dysfunction in the early phase of AMI (Bennett and Boyle 1998;Mayr and Xu 2001;Toga et al 2007).…”

Remote Ischemic Preconditioning: A Novel Protective Method From Ischemia Reperfusion Injury—A Review

“…In three studies in RIPC, Tanaka et al showed in a rabbit model RIPC by four cycles of 5 min CAO and 5 min reperfusion [21,131] increased cardiac tolerance due to increased HSP expression in the ischemic and remote myocardium; Konstantinov showed RIPC by six cycles of 4 min femoral artery occlusion and 4 min reperfusion increased expression of HSP73 genes (antiinflammatory) in the heart of preconditioned mice as compared to sham [40] and Chen et al in a rat model showed increased myocardial HSP expression (HSP70) following hindlimb RIPC [76].…”

Repeated remote ischemic conditioning attenuates left ventricular remodeling via exosome-mediated intercellular communication on chronic heart failure after myocardial infarction

“…They reported that ischemic preconditioning in the left circumflex coronary artery attenuated ischemia-reperfusion (IR) injury by subsequent occlusion of the left anterior descending coronary artery (LAD). Thereafter, some reports have shown that ischemic preconditioning [8,9] and postconditioning [10,11] of the extremities can protect the heart from IR injury. Thus, remote ischemic conditioning (RIC) may be one of the therapeutic strategies for protecting organs or tissue against IR injury.…”