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Muscle microvascular oxygenation in chronic heart failure: role of nitric oxide availability
Author(s) -
Ferreira L. F.,
Hageman K. S.,
Hahn S. A.,
Williams J.,
Padilla D. J.,
Poole D. C.,
Musch T. I.
Publication year - 2006
Publication title -
acta physiologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.591
H-Index - 116
eISSN - 1748-1716
pISSN - 1748-1708
DOI - 10.1111/j.1748-1716.2006.01598.x
Subject(s) - nitric oxide , sodium nitroprusside , heart failure , medicine , endocrinology , chemistry , oxygenation , cardiology , anesthesia
Aim: To test the hypothesis that diminished vascular nitric oxide availability might explain the inability of individuals with chronic heart failure (CHF) to maintain the microvascular PO 2 ’s ( PO 2mv ∝ O 2 delivery‐to‐uptake ratio) seen in healthy animals. Methods: We superfused sodium nitroprusside (SNP; 300 μ m ), Krebs–Henseleit (control, CON) and l ‐nitro arginine methyl ester ( l ‐NAME; 1.5 m m ) onto the spinotrapezius muscle and measured PO 2mv by phosphorescence quenching in female Sprague–Dawley rats ( n = 26) at rest and during twitch contractions (1 Hz). Seven rats served as controls (Sham) while CHF was induced by myocardial infarction. CHF rats were grouped as moderate (MOD; n = 15) and severe CHF (SEV; n = 4) according to morphological data and baseline PO 2mv . Results: In contrast to Sham and MOD, l ‐NAME did not affect the PO 2mv response (dynamics and steady‐state) of SEV when compared with CON. SNP restored the PO 2mv profile of SEV to that seen in Sham animals during CON. Specifically, the effect of l ‐NAME expressed as Δ( l ‐NAME – CON) were: Baseline PO 2mv [in mmHg, ΔSham = −7.0 ± 1.6 ( P < 0.05); ΔSEV =−1.2 ± 2.1], end‐contractions PO 2mv [in mmHg, ΔSham = −5.0 ± 1.0 ( P < 0.05); ΔSEV = −2.5 ± 0.5] and time constant of PO 2mv decrease [in s, ΔSham = −6.5 ± 3.0 ( P < 0.05); ΔSEV = −3.2 ± 1.8]. Conclusion: These data provide the first direct evidence that the pathological profiles of PO 2mv associated with severe CHF can be explained, in part, by a diminished vascular NO availability.