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This Article Full Text Full Text (PDF) All Versions of this Article: 293/1/H846    most recent 00156.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Di Vanna, A. Articles by Negrão, C. E. Search for Related Content PubMed PubMed Citation Articles by Di Vanna, A. Articles by Negrão, C. E.

Blunted muscle vasodilatation during chemoreceptor stimulation in patients with heart failure

¹Heart Institute (InCor), University of São Paulo Medical School, and ²School of Physical Education and Sport, University of São Paulo, São Paulo, Brazil; and ³Department of Cardiology, University of California Los Angeles, Los Angeles, California

Submitted 7 February 2007 ; accepted in final form 11 April 2007

Chemoreflex control of sympathetic nerve activity is exaggerated in heart failure (HF) patients. However, the vascular implications of the augmented sympathetic activity during chemoreceptor activation in patients with HF are unknown. We tested the hypothesis that the muscle blood flow responses during peripheral and central chemoreflex stimulation would be blunted in patients with HF. Sixteen patients with HF (49 ± 3 years old, Functional Class II-III, New York Heart Association) and 11 age-paired normal controls were studied. The peripheral chemoreflex control was evaluated by inhalation of 10% O₂ and 90% N₂ for 3 min. The central chemoreflex control was evaluated by inhalation of 7% CO₂ and 93% O₂ for 3 min. Muscle sympathetic nerve activity (MSNA) was directly evaluated by microneurography. Forearm blood flow was evaluated by venous occlusion plethysmography. Baseline MSNA were significantly greater in HF patients (33 ± 3 vs. 20 ± 2 bursts/min, P = 0.001). Forearm vascular conductance (FVC) was not different between the groups. During hypoxia, the increase in MSNA was significantly greater in HF patients than in normal controls (9.0 ± 1.6 vs. 0.8 ± 2.0 bursts/min, P = 0.001). The increase in FVC was significantly lower in HF patients (0.00 ± 0.10 vs. 0.76 ± 0.25 units, P = 0.001). During hypercapnia, MSNA responses were significantly greater in HF patients than in normal controls (13.9 ± 3.2 vs. 2.1 ± 1.9 bursts/min, P = 0.001). FVC responses were significantly lower in HF patients (–0.29 ± 0.10 vs. 0.37 ± 0.18 units, P = 0.001). In conclusion, muscle vasodilatation during peripheral and central chemoreceptor stimulation is blunted in HF patients. This vascular response seems to be explained, at least in part, by the exaggerated MSNA responses during hypoxia and hypercapnia.

chemoreflex sensitivity; sympathetic nerve activity; forearm blood flow