| Autor: |
Sperandio, Priscila A., Oliveira, Mayron F., Rodrigues, Miguel K., Berton, Danilo C., Treptow, Erika, Nery, Luiz E., Almeida, Dirceu R., Neder, J. Alberto |
| Zdroj: |
American Journal of Physiology: Heart & Circulatory Physiology; Dec2012 Part2, Vol. 303 Issue 12, pH1474-H1480, 7p |
| Abstrakt: |
Nitric oxide (NO) can temporally and spatially match microvascular oxygen (O2) delivery (QO2mv) to O2 uptake (VO2) in the skeletal muscle, a crucial adjustment-to-exercise tolerance that is impaired in chronic heart failure (CHF). To investigate the effects of NO bioavailability induced by sildenafil intake on muscle QO2mv-to-O2 utilization matching and VO2 kinetics, 10 males with CHF (ejection fraction =27± 6%) undertook constant work-rate exercise (70-80% peak). Breath-bybreath VO2, fractional O2 extraction in the vastus lateralis ([deoxygenated hemoglobin +myoglobin ([deoxy-Hb + Mb]) by nearinfrared spectroscopy}, and cardiac output (CO) were evaluated after sildenafil (50 mg) or placebo. Sildenafil increased exercise tolerance compared with placebo by ~20%, an effect that was related to faster onand off-exercise VO2 kinetics (P < 0.05). Active treatment, however, failed to accelerate CO dynamics (P < 0.05). On-exercise [deoxy-Hb + Mb] kinetics were slowed by sildenafil (~25%), and a subsequent response "overshoot" (n = 8) was significantly lessened or even abolished. In contrast, [deoxy-Hb + Mb] recovery was faster with sildenafil (~15%). Improvements in muscle oxygenation with sildenafil were related to faster on-exerciseVO2 kinetics, blunted oscillations in ventilation (n = 9), and greater exercise capacity (P < 0.05). Sildenafil intake enhanced intramuscular QO2mv-to-VO2 matching with beneficial effects onVO2 kinetics and exercise tolerance in CHF. The lack of effect on CO suggests that improvement in blood flow to and within skeletal muscles underlies these effects. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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