Cardiac myocardium exposed to such sublethal stress as a brief period of ischemia or whole-body hyperthermia resists to ischemia/reperfusion injury (preconditioning effect). Heat shock protein 70 (HSP 70) and manganese superoxide dismutase (MnSOD) may have a role in this mechanism. The aim of this study was to demonstrate the expression of HSP 70 and MnSOD activity in the myocardium of rabbit at 4 hours after ischemic preconditioning and compare them with heat shock model.

The experimental procedures were undergone in seventeen New Zealand white rabbits. Ischemic preconditioning was performed through three 3-minute episodes of coronary ligation separated by 5 minutes of reperfusion. Whole-body hyperthermia (rectal temperature was raised to 42 Celsius degrees for 15 minutes by wrapping rabbits in an electric warming blanket) was treated to heat shock group. Control rabbits did not undergo ischemic preconditioning or whole-body hyperthermia. Immunohistochemical staining for demonstrating HSP 70 was done with monoclonal antibody. The activity of MnSOD was examined with SOD-525 kit.

In ischemic preconditioning group, myocardial HSP 70 expression was significantly increased in ischemic area compared with non-ischemic area (P<0.01). HSP 70 expression in ischemic area was more increased in both ischemic preconditioning and heat shock group(P<0.01) versus the control group. The same trend was observed in non-ischemic area (P<0.01). In ischemic preconditioning group, the activity of MnSOD was significantly enhanced in ischemic area compared with non-ischemic area (3.82±0.15 vs 0.11±0.16, P<0.05). The MnSOD activity was more enhanced in ischemic area of ischemic preconditioning group than in both heat shock and control group (3.82±0.15 vs 0.67±0.72, 0.65±0.29, P<0.05).

We found difference between ischemic preconditioning and heat shock in the level of expression of HSP 70 and activity of MnSOD. Both preconditioning effect may have different mechanism on myocardial tolerance to ischemia/reperfusion injury.