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A3921 - Does the Carotid Chemoreceptor Play a Role in Cardiopulmonary Regulation, Dyspnea and Exercise Intolerance in COPD?
Author Block: D. Phillips, S. E. Collins, T. L. Bryan, E. Y. Wong, M. S. McMurtry, M. Bhutani, M. K. Stickland; University of Alberta, Edmonton, AB, Canada.
RATIONALE: COPD patients have an exaggerated ventilatory response to exercise, contributing to exertional dyspnea and exercise intolerance, however, the reasons are not well understood. We have recently demonstrated enhanced activity and sensitivity of the carotid chemoreceptor (CC) in COPD which may alter cardiopulmonary responses to exercise, exertional dyspnea and exercise intolerance. Accordingly, we sought to examine whether CC inhibition improves cardiovascular and ventilatory responses, dyspnea and exercise tolerance in COPD. METHODS: In a randomized double blind crossover study, six COPD patients (FEV1 predicted ± SD: 82 ± 19%) and fourteen healthy controls completed two time to symptom limitation (TLIM) constant load exercise tests at 75% peak power output with either intravenous saline or low-dose dopamine (2 μg/kg/min). Dopamine has been previously shown to inhibit the CC. Ventilatory responses were evaluated using expired gas data and dyspnea was evaluated using a modified Borg scale. Inspiratory capacity maneuvers were performed to determine operating lung volumes. Cardiac output (impedance cardiography), arterial O2 saturation (pulse oximetry) and haemoglobin concentration (venous blood sampling) were collected to estimate oxygen delivery. Vascular conductance was calculated as cardiac output/mean arterial pressure (MAP). RESULTS: At a standardized exercise time (isotime) of 4 minutes and at TLIM, minute ventilation was not different between saline and dopamine conditions in COPD (isotime 50.2 ± 4.0 vs 49.3 ± 4.3 L/min, p=0.35; TLIM 56.5 ± 4.1 vs 60.0 ± 4.5 L/min, p=0.30) or controls (isotime 72.6 ± 7.0 vs 69.7 ± 5.2 L/min, p=0.24; TLIM 88.3 ± 8.3 vs 88.0 ± 7.8 L/min, p=0.92). Operating lung volumes, exertional dyspnea and oxygen delivery were not different between conditions within either group. Vascular conductance was increased with dopamine, secondary to reduced MAP, in COPD (isotime 97.5 ± 12.2 vs 108.3 ± 11.5 ml/min/mmHg, p=0.04; TLIM 99.5 ± 12.1 vs 115.8 ± 15.6 ml/min/mmHg, p=0.04), while no change was observed in controls (isotime 109.0 ± 6.5 vs 116.0 ± 8.5 ml/min/mmHg, p=0.20; TLIM 121.0 ± 9.2 vs 131.0 ± 10.2 ml/min/mmHg, p=0.09). There was no change in time to exhaustion in either group with dopamine (COPD 9.1 ± 2.2 vs 10.8 ± 3.2 min, p=0.63; Control 11.0 ± 1.1 vs 12.4 ± 1.2 min, p=0.14). CONCLUSION: Preliminary data suggest that the CC plays a role in cardiovascular regulation during exercise in COPD; however, ventilation, dyspnea and exercise intolerance were unaffected by CC inhibition in COPD patients.