JOURNAL ARTICLE
RESEARCH SUPPORT, N.I.H., EXTRAMURAL
RESEARCH SUPPORT, NON-U.S. GOV'T
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Vascular K ATP channels mitigate severe muscle O 2 delivery-utilization mismatch during contractions in chronic heart failure rats.

The vascular ATP-sensitive K+ (KATP ) channel is a mediator of skeletal muscle microvascular oxygenation (PO2 mv) during contractions in health. We tested the hypothesis that KATP channel function is preserved in chronic heart failure (CHF) and therefore its inhibition would reduce PO2 mv and exacerbate the time taken to reach the PO2 mv steady-state during contractions of the spinotrapezius muscle. Moreover, we hypothesized that subsequent KATP channel activation would oppose the effects of this inhibition. Muscle PO2 mv (phosphorescence quenching) was measured during 180s of 1-Hz twitch contractions (∼6V) under control, glibenclamide (GLI, KATP channel antagonist; 5mg/kg) and pinacidil (PIN, KATP channel agonist; 5mg/kg) conditions in 16 male Sprague-Dawley rats with CHF induced via myocardial infarction (coronary artery ligation, left ventricular end-diastolic pressure: 18±1mmHg). GLI reduced baseline PO2 mv (control: 28.3±0.9, GLI: 24.8±1.0mmHg, p<0.05), lowered mean PO2 mv (average PO2 mv during the overall time taken to reach the steady-state; control: 20.6±0.6, GLI: 17.6±0.3mmHg, p<0.05), and slowed the attainment of steady-state PO2 mv (overall mean response time; control: 66.1±10.2, GLI: 93.6±7.8s, p<0.05). PIN opposed these effects on the baseline PO2 mv, mean PO2 mv and time to reach the steady-state PO2 mv (p<0.05 for all vs. GLI). Inhibition of KATP channels exacerbates the transient mismatch between muscle O2 delivery and utilization in CHF rats and this effect is opposed by PIN. These data reveal that the KATP channel constitutes one of the select few well-preserved mechanisms of skeletal muscle microvascular oxygenation control in CHF.

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