Submitted on February 7, 2007
Accepted on April 11, 2007
Blunted Muscle Vasodilatation During Chemoreceptor Stimulation in Patients with Heart Failure
Andrea Di Vanna1, Ana MFW Braga2, Mateus C Laterza2, Linda M Ueno2, Maria UPB Rondon2, Antonio CP Barretto2, Holly R. Middlekauff3, and Carlos Eduardo Negrao4*
1 Heart Institute (InCor), University of São Paulo, Medical School, Sao Paulo, SP, Brazil
2 Heart Institute (InCor), University of São Paulo, Medical School, Sao Paulo, SP, Brazil; Sao Paulo, SP, Brazil
3 Department of Medicine/Cardiology, 47-123 CHS, University of California-Los Angeles School of Medicine, Los Angles, California, United States
4 Heart Institute (InCor), University of Sao Paulo Medical School, Sao Paulo, Sao Paulo, Brazil; School of Physical Education and Sport, University of Sao Paulo, Sao Paulo, SP, Brazil
* To whom correspondence should be addressed. E-mail: cndnegrao{at}incor.usp.br.
Chemoreflex control of sympathetic nerve activity is exaggerated in heart failure(HF) patients. However, the vascular implications of the augmented sympathetic activity during chemoreceptors 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, NYHA) and 11 age-paired normal controls were studied. The peripheral chemoreflex control was evaluated by inhalation of 10% O2 and 90% N2 during 3 minutes. The central chemoreflex control was evaluated by inhalation of 7% CO2 and 93% O2 during 3 minutes. 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 U, 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 U, P=0.001). In conclusion, muscle vasodilatation during peripheral and central chemoreceptors 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.
