The myocardial heat shock response following sodium salicylate treatment

In cultured cells, salicylate has been shown to potentiate the induction of Hsp72 so that a mild heat stress (40 degreesC) in the presence of salicyla te induces an Hsp72 response that is similar to a severe heat stress (42 de greesC). To determine whether salicylate can potentiate the myocardial Hsp7 0 response in vivo and confer protection from an ischemic stress, male Spra gue-Dawley rats (250-300 g) were placed into 5 groups: (1) control, (2) sal icylate only (400 mg/kg), (3) mild heat stress (40 degreesC for 15 minutes) , (4) mild heat stress plus salicylate, and (5) severe heat stress (42 degr eesC for 15 minutes). Twenty-four hours following salicylate treatment and/ or heat stress, animals were anesthetized, their hearts rapidly isolated, a nd hemodynamic function evaluated using the Langendorff technique. Hsp72 co ntent was subsequently assessed by Western blotting. Although salicylate in combination with a mild heat stress induced heat shock factor activation, only the hearts from severely heat-stressed animals (42 degreesC) demonstra ted a significantly elevated myocardial Hsp72 content and a significantly e nhanced postischemic recovery of left ventricular developed pressure and ra tes of contraction and relaxation. These results support the role for Hsp72 as a protective protein and suggest that neither salicylate treatment alon e nor salicylate in combination with a mild heat stress potentiates the myo cardial Hsp72 response.