Whole body heat shock fails to protect mouse heart against ischemia/reperfusion injury: Role of 72 kDa heat shock protein and antioxidant enzymes

The transgenic mice overexpressing heat shock protein 72 (HSP72) or antioxi dants have been reported to be more resistant to myocardial ischemia/ reper fusion injury. However, it remains unknown whether whole body heat stress ( HS) which may induce HSP 72 or endogenous antioxidants affords similar prot ection in the mouse heart. Adult male mice were treated with either HS (42 degrees C for 15 min) or anesthesia only (SC) against a group of non-stress ed controls (NC). At 6 or 24 h later, the hearts were excised and perfused at a constant pressure of 55 mmHg in Langendorff mode. Following 30 min equ ilibration, hearts were subjected to 20 min of global ischemia and 30 min r eperfusion (37 degrees C). Ventricular force was measured by a force-displa cement transducer attached to the apex. Leakage of intracellular enzymes (C K, LDH) was measured in coronary efflux. Infarct size was determined by tet razolium staining. The results showed that no significant differences betwe en HS, SC, and NC groups in Ventricular contractile function, CK and LDH re lease, or infarct size were observed at either time window. HS enhanced the expression of HSP72 in mouse hearts by two- to three-fold, whereas antioxi dant enzyme activities (catalase and MnSOD) did not change significantly, W e conclude that HS does not precondition the isolated perfused mice hearts against ischemia/reperfusion injury, despite induction of HSP72. (C) 1998 A cademic Press.