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Chronic heart failure (CHF) alters nNOS‐mediated control of skeletal muscle contractile function
Author(s) -
Copp Steven,
Hirai Daniel M,
Ferguson Scott K,
Holdsworth Clark T,
Poole David C,
Musch Timothy I
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.860.19
Subject(s) - medicine , preload , skeletal muscle , isometric exercise , endocrinology , chemistry , heart failure , vasodilation , muscle contraction , steady state (chemistry) , hemodynamics
Neuronal NO synthase (nNOS)‐derived NO modulates skeletal muscle contractile function. It is unknown if altered nNOS function contributes to the muscle contractile dysfunction in CHF. We tested the hypothesis that nNOS‐mediated control of skeletal muscle contractile function and economy is impaired in CHF rats. Spinotrapezius muscles were exteriorized and linked to a force transducer in 5 healthy (LVEDP: 6±1 mmHg) and 4 CHF (coronary artery ligation, LVEDP: 13±1 mmHg) rats. Force was measured during 3 min of electrically‐induced 1 Hz (~6–8 V) twitch contractions pre‐ and post‐nNOS inhibition with SMTC (0.56 mg/kg i.a.). Muscle VO 2 was calculated (Fick equation) from measured blood flow (radiolabelled microspheres), arterial O 2 content, and microvascular Po 2 (phosphorescence quenching). Healthy : SMTC elevated the force‐time integral (+8%) and reduced contracting steady‐state VO 2 (−17%). SMTC elevated the steady‐state force/VO 2 ratio (60±20 g/ml/min, P <0.05). CHF : SMTC did not alter the force‐time integral or contracting steady‐state VO 2 . Moreover, SMTC did not change steady‐state Δ force/VO 2 ratio (−10±60 g/ml/min, P >0.05). The nNOS‐derived NO modulation of skeletal muscle function present in healthy rats is attenuated in CHF rats indicating CHF‐induced alterations in the control mechanisms regulating contractile function. (AHA Midwest Affiliate, NIH‐HL‐108328)