Key result
Treatment with trandolapril in rats with chronic heart failure reversed the failure of myocardial Hsp72 and Hsp73 production and prevented the decline in rate pressure product after hyperthermia.
Why the study?
Does trandolapril improve Hsp72 and Hsp73 production and myocardial contractile function after hyperthermia in rats with chronic heart failure following myocardial infarction?
Population
Rats with chronic heart failure following acute myocardial infarction induced by coronary artery ligation
Comparison
Trandolapril 3 mg/kg/day from the 2nd to 8th… vs Untreated rats with CAL and sham-operated rats
Design
Preclinical
Follow-up
8 weeks
Authors
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Does not support clinical use; leaves open whether ACE inhibition preserves Hsp responses in human heart failure.
Does trandolapril improve Hsp72 and Hsp73 production and myocardial contractile function after hyperthermia in rats with chronic heart failure following myocardial infarction?
Trandolapril preserves the ability of the failing heart to induce Hsp72 and Hsp73 production, which may increase tolerance against heat stress-induced deterioration of myocardial contractile function.
Tanonaka et al. (2001) studied Chronic heart failure following acute myocardial infarction. Trandolapril vs. Non-treated rats with coronary artery ligation / sham-operated rats was evaluated on Rate pressure product (RPP) decline and Hsp72/Hsp73 production after hyperthermia. Treatment with trandolapril in rats with chronic heart failure reversed the failure of myocardial Hsp72 and Hsp73 production and prevented the decline in rate pressure product after hyperthermia.
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