Abstract
NO bioavailability has been implicated in the muscle microvascular dysfunction of CHF at rest and during contractions.PURPOSETo test the hypothesis that differences in the O2 delivery/utilization balance, which sets the microvascular O2 partial pressure (PO2mv), between control (C) and severe CHF rats following the onset of contractions are due substantially to NO reduction.METHODSPO2mv was measured via phosphorescence quenching in the spinotrapezius muscle of 6 C and 4 CHF rats (male Sprague‐Dawley, 7‐10 wk post‐myocardial infarction, LVEDP 35+2 mmHg). Separate electrically‐induced contraction bouts (1 Hz) were performed with superfusion of SNP (300 μmol), Krebs‐Henseleit buffer (KH), and L‐NAME (1.5 mmol). The area under the PO2mv profile (PO2AREA) was calculated from 0‐60 s of each bout (expressed below as mmHg·s/min).RESULTSFor KH, C had a greater (P < 0.05) PO2AREA (1042 ± 62) than CHF (721 ± 141). SNP increased PO2AREA (C: 1371 ± 59, CHF: 1263 ± 97, P > 0.05) whereas L‐NAME reduced PO2AREA (C: 613 ± 74, CHF: 416 ± 70, P > 0.05) to equivalent values in C and CHF rats.CONCLUSIONSThis demonstrates, for the first time, that the impaired muscle microvascular O2 delivery/utilization balance in CHF is eliminated by increasing (SNP) or removing (L‐NAME) NO bioavailability suggesting that the dysfunctional CHF PO2mv profile results principally from endogenous NO alterations.AHA, Heartland Affiliate 0750090Z
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