Key result
Quinidine, procaine amide, and diphenylhydantoin inhibited the incorporation of tritiated leucine into myocardial proteins in rats, whereas lidocaine and propranolol did not.
Population
Rat model (in vitro and in vivo)
Design
Preclinical
Authors
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May link select antiarrhythmics to myocardial depression via protein synthesis inhibition in rats; leaves open human relevance.
Certain antiarrhythmic agents (quinidine, procaine amide, diphenylhydantoin) inhibit myocardial protein synthesis in rat models, which may relate to their myocardial depressant effects.
Beller et al. (1969) studied this question. Quinidine, procaine amide, and diphenylhydantoin vs. Lidocaine or propranolol was evaluated on Incorporation of tritiated leucine into myocardial proteins. Quinidine, procaine amide, and diphenylhydantoin inhibited the incorporation of tritiated leucine into myocardial proteins in rats, whereas lidocaine and propranolol did not.
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