In vivo heat shock preconditioning mitigates calcium overload during ischaemia/reperfusion in the isolated, perfused rat heart

Heat shock (HS) pretreatment of the heart is effective in mitigating the deleterious effects of ischaemia/ reperfusion. The main objective of this study was to determine whether the beneficial effect of HS is associated with the preservation of intracellular Ca2+ handling in the ischaemic/reperfused, isolated rat heart. Twenty-four hours after raising body core temperature to 42 degreesC for 15 min, rat hearts were perfused according to Langendor. and subjected to 30 min ischaemia followed by 20 min reperfusion. Cyclic changes of cytoplasmic calcium ion [Ca-i(2+)] levels were measured by surface fluorometry using Indo-1AM. Reperfused HS hearts showed improved recovery of contractile function compared with control hearts: end-diastolic pressure: 45 +/- 11 vs. 64 +/- 22 mm Hg; developed pressure: 72 +/- 12 vs. 41 +/- 20 mm Hg; maximum rate of pressure increase (+ d P/d t(max)): 1,513 +/- 305 vs. 938 +/- 500 mm Hg/s; maximum rate of pressure decrease (-d P/d t(max)): -1,354 +/- 304 vs. -806 +/- 403 mm Hg/s. HS hearts displayed a significantly lower end-diastolic cytosolic [Ca2+] ([Ca2+](i)) after reinstallation of flow. The dynamic parameters of the Ca-i(2+) transients, i.e. the maximum rate of increase/decrease (+/- dCa(2+) (i)/d t(max)) and amplitude, did not differ between reperfused control and HS hearts. The novel finding of this study is that improved performance of the HS-pre-conditioned heart after an ischaemic insult is associated with a reduced end-diastolic Ca-i(2+) load, and most likely, preserved Ca2+ sensitivity of the myocardial contractile machinery