Muscle microvascular oxygenation in chronic heart failure: role of nitric oxide availability

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 PO2’s (PO2mv ∝ O2 delivery‐to‐uptake ratio) seen in healthy animals. Methods: We superfused sodium nitroprusside (SNP; 300 μm), Krebs–Henseleit (control, CON) and l‐nitro arginine methyl ester (l‐NAME; 1.5 mm) onto the spinotrapezius muscle and measured PO2mv 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 PO2mv. Results: In contrast to Sham and MOD,l‐NAME did not affect the PO2mv response (dynamics and steady‐state) of SEV when compared with CON. SNP restored the PO2mv 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 PO2mv [in mmHg, ΔSham = −7.0 ± 1.6 (P