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July 14, 1998Circulation

Heterogeneous Expression and Activity of Endothelial and Inducible Nitric Oxide Synthases in End-Stage Human Heart Failure

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NOS isoform expression in failing hearts is hypothesis-generating; leaves open etiology- and therapy-specific roles pending controlled studies.

To determine the cellular localization and enzymatic activity of endothelial and inducible nitric oxide synthases in end-stage human heart failure relative to etiology and beta-adrenergic medication.
Examined myocardial tissue samples obtained from 28 failing human hearts with diverse etiologies and 4 nonfailing control hearts.
Assessed eNOS and iNOS protein presence, mRNA hybridization signals, and catalytic activity in relation to myocardial lesions and preoperative beta-adrenergic therapy.
Subendocardial cardiac myocytes exhibited elevated eNOS expression in failing hearts, with signals being more pronounced in patients receiving beta-blockers and diminished in those receiving beta-agonists.
Myocyte iNOS expression occurred consistently across multiple heart failure etiologies, but pronounced iNOS signals were concentrated in infiltrating macrophages within infarcted, myocarditic, and septic tissues.
Total iNOS enzymatic activity varied widely across failing hearts and correlated significantly with the density of infiltrating macrophages rather than myocyte expression alone.

Fukuchi et al. (1998) studied this question.

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NOS isoform expression in failing hearts is hypothesis-generating; leaves open etiology- and therapy-specific roles pending controlled studies.