Effects of oxygen on autonomic nervous system dysfunction in patients with chronic obstructive pulmonary disease.
Chronic hypoxaemia can play a pathological role in abnormalities of the autonomic nervous system (ANS). In patients with chronic obstructive pulmonary disease (COPD), chronic hypoxaemia is associated with increased mortality and only long-term oxygen therapy is able to improve their survival. Normoxaemic COPD patients have been shown to suffer from abnormalities in ANS function. The aims of this study were to evaluate ANS function in COPD patients with chronic hypercapnic respiratory insufficiency and to test whether oxygen supplementation could reverse any ANS dysfunction. Eleven stable COPD patients with chronic hypercapnic respiratory insufficiency underwent evaluation of ANS by analysis of variability in cardiac frequency at rest and during both vagal (controlled breathing) and sympathetic (tilting) stimuli breathing with and without oxygen supplementation. Thirteen male, healthy, nonsmoking volunteers served as controls. Evaluation of ANS in COPD patients during hypoxic conditions showed alterations both at rest and in response to vagal and sympathetic stimuli. Oxygen supply reversed hypoxaemia without significant changes in arterial carbon dioxide tension and, therefore, ANS alterations were corrected during sympathetic stimulus only. Breathing room air and oxygen, the resting low-frequency (LF) powers were 45+/-15 and 148+/-55 ms2 x Hz(-1), respectively, and controlled breathing LF were 107+/-41 and 141+/-113 ms2 x Hz(-1), respectively. In stable patients with chronic obstructive pulmonary disease with chronic respiratory insufficiency, hypoxaemia is associated with derangements in the autonomic nervous system which may be partially reversed by oxygen administration.
Scalvini
S
S
Dept of Cardiology, Salvatore Maugeri Foundation IRCCS, Gussago, Italy.
Porta
R
R
Zanelli
E
E
Volterrani
M
M
Vitacca
M
M
Pagani
M
M
Giordano
A
A
Ambrosino
N
N
D000368:Aged; D001341:Autonomic Nervous System / Q000187:drug effects* / Q000503:physiopathology*; D005260:Female; D006801:Humans; D006935:Hypercapnia / Q000188:drug therapy / Q000503:physiopathology*; D008173:Lung Diseases, Obstructive / Q000503:physiopathology*; D008297:Male; D010100:Oxygen / Q000494:pharmacology* / Q000627:therapeutic use
D010100:Oxygen