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Response to hypoxia of pulmonary arteries in chronic obstructive pulmonary disease: an in vitro study

Depts of Pulmonary Medicine and Pathology, Institut d'Investigacions Biomèdiques Pi i Sunyer (IDIBAPS), Hospital Clínic, Universitat de Barcelona, Barcelona, Spain

CORRESPONDENCE: J.A. Barberà, Servei de Pneumologia, Hospital Clínic, Villarroel, 170, 08036, Barcelona, Spain. Fax: 34 932275455. E-mail: jbarbera@clinic.ub.es.

Keywords: chronic airflow obstruction, endothelial function, gas exchange, hypoxic pulmonary vasoconstriction, lung, nitric oxide

Received: January 17, 2002
Accepted March 12, 2002

This study was supported by Grants 99/0188 and 00/0922 from the Fondo de Investigación Sanitaria, and SEPAR-2000 from the Sociedad Española de Neumología y Cirugía Torácica. V.I. Peinado is supported by the Comissió Interdepartamental de Recerca i Innovació Tecnològica and the Fundació Clínic per a la Recerca Biomèdica. S. Santos is the recipient of a Research Fellowship Award from the Sociedad Española de Neumología y Cirugía Torácica (SEPAR).

Patients with chronic obstructive pulmonary disease (COPD) show impaired hypoxic pulmonary vasoconstriction that might contribute to abnormal gas exchange and could be related to endothelial dysfunction in pulmonary arteries. The aim of the study was to investigate the response of PA to hypoxic stimulus in vitro in COPD, and the role of endothelium-derived nitric oxide (NO) in this response.

The pulmonary arteries of 25 patients who underwent lung resection were studied. Patients were divided into controls, COPD+normoxaemia (COPD_N) and COPD+hypoxaemia (COPD_H). Hypoxic vasoconstriction (HV) was evaluated before and after stimulation or inhibition of the endothelial release of NO, and in the presence of exogenous NO.

Compared with the other groups, HV was reduced in COPD_H. The magnitude of HV correlated with the oxygen tension in arterial blood. The hypoxic stimulus induced greater contraction after stimulating endothelial release of NO, whereas its inhibition practically abolished HV. Exogenous NO completely inhibited HV. Maximal relaxation induced by endothelium-dependent vasodilators correlated with the magnitude of HV.

In conclusion, pulmonary arteries of patients with chronic obstructive pulmonary disease and hypoxaemia have an impaired response to hypoxic stimulus, and the endothelial release of nitric oxide modulates hypoxic vasoconstriction. The depressed response of pulmonary arteries to hypoxia may contribute to abnormal gas exchange in chronic obstructive pulmonary disease.

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