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Am J Physiol Heart Circ Physiol 279: H836-H843, 2000;
0363-6135/00 $5.00
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Vol. 279, Issue 2, H836-H843, August 2000

Glucocorticoid pretreatment protects cardiac function and induces cardiac heat shock protein 72

Guro Valen1, Tsutomu Kawakami1, Peeter Tähepôld1, Alexandra Dumitrescu1, Christian Löwbeer2, and Jarle Vaage3

1 Crafoord Laboratory of Experimental Surgery, 3 Department of Thoracic Surgery, Karolinska Hospital, S-171 76 Stockholm; and 2 Department of Clinical Chemistry, Huddinge University Hospital, 141 86 Huddinge, Sweden

Acute administration of glucocortiocoids reduces inflammation. Increasing knowledge of the mechanisms of action indicate that pretreatment with glucocorticoids could have organ-protective effects. We investigated whether pretreatment with methylprednisolone (MP) protected the heart against ischemia-reperfusion dysfunction, and we hypothetized that this protection might be due to induction of the cardioprotective heat shock protein 72 (HSP72). Rats were given vehicle or MP-40 mg/kg im as a double injection starting either 24 or 120 h (5 days) before their hearts were excised for Langendorff perfusion (n = 6-11 hearts in each group). MP improved left ventricular function and coronary flow during reperfusion after 30 min of global ischemia and reduced infarct size. Cardiac HSP72 gradually increased in a 24-h time course after MP treatment, and the increase was sustained 5 days afterward (immunoblotting). HSP72 mRNA was either reduced or unchanged, indicating a posttranscriptional regulation. Pretreatment with hydrocortisone or dexamethasone (n = 7-8 hearts of each) similarily increased cardiac HSP72 24 h afterward. This paper demonstrates that glucocorticoids increase cardiac HSP72 and protect organ function against ischemia-reperfusion injury.

methylprednisolone; dexamethasone; hydrocortisone; ischemia-reperfusion


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