Key result
Systemic administration of L-NAME at 1 and 10 mg/kg decreased myocardial O2 consumption by an average of 23 +/- 3.8% and 34 +/- 7.2%, respectively, in intact dogs.
Blockade of NO synthesis reduces myocardial oxygen consumption and segment shortening in vivo, indicating that endogenous NO augments contractile performance.
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Endogenous NO may augment myocardial performance in vivo; leaves open translation to human energetics or therapy.
Sherman et al. (1997) studied this question. Blockade of NO synthase (L-NAME or N omega-nitro-L-arginine) was evaluated on Myocardial O2 consumption. Systemic administration of L-NAME at 1 and 10 mg/kg decreased myocardial O2 consumption by an average of 23 +/- 3.8% and 34 +/- 7.2%, respectively, in intact dogs.
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