beta-endorphin and Lung-Diseases--Obstructive

To determine whether beta-endorphin plays a role in the regulation of pulmonary vascular tone in patients with pulmonary hypertension, we investigated the relations between hemodynamics and beta-endorphin and adenosine concentrations in 3 clinical situations: (1) normal hemodynamics (7 subjects, mean pulmonary artery [PA] pressure 18.5 +/- 1 mm Hg); (2) moderate pulmonary hypertension secondary to chronic obstructive pulmonary disease (COPD) (8 patients, mean PA pressure 31 +/- 3 mm Hg); and (3) severe primary pulmonary hypertension (PPH) (8 patients, mean PA pressure 70 +/-5 mm Hg). Plasma beta-endorphin and adenosine were measured in a distal PA and in the femoral artery in room air and during oxygen inhalation. Beta-endorphin levels were similar in the pulmonary and systemic circulations. No difference was observed between patients with COPD and PPH, but relative to controls, both had significantly higher beta-endorphin levels. Pulmonary adenosine was significantly lower in patients with pulmonary hypertension than in controls (-60% in COPD [p <0.005] and -70% in PPH [p <0.001]). Pure oxygen administration significantly decreased adenosine and beta-endorphin levels, much more so in patients with COPD and PPH. We found a negative correlation between beta-endorphin and adenosine concentrations (r = -0.751, p <0.001): the higher the adenosine, the lower the beta-endorphin level. These observations suggest that because adenosine release by pulmonary vascular endothelium is reduced in pulmonary hypertension, the resulting worsened hypoperfusion and tissue oxygenation may cause increased beta-endorphin release.

Topics: Adenosine; Adult; beta-Endorphin; Biomarkers; Blood Gas Analysis; Female; Humans; Hypertension, Pulmonary; Lung Diseases, Obstructive; Male; Middle Aged; Oxygen Inhalation Therapy; Prognosis; Pulmonary Wedge Pressure; Radioimmunoassay

The present study is concerned with plasma beta-endorphin and glucose tolerance in patients with chronic obstructive pulmonary disease (COPD). Plasma beta-endorphin, glucagon and insulin concentrations were measured during an oral glucose tolerance test in 20 COPD patients and in 18 age-matched healthy controls (mean age 62 years). Seven patients had a moderate COPD (group I) and seven a severe COPD (group II). The remaining six severe COPD patients received long-term oxygen therapy (group III). We found that fasting levels of beta-endorphin were significantly increased in all patient groups compared to healthy controls (p < 0.01, 0.05 and 0.005, respectively). Six of the 13 severely diseased COPD patients had impaired glucose tolerance. Plasma beta-endorphin levels decreased significantly during OGTT in the COPD patients (p < 0.05). Fasting beta-endorphin levels were higher in patients with impaired glucose tolerance than in those patients with normal OGTT (42.0 pmol/L +/- 11.4 SD versus 34.8 +/- 10.2). However, this difference was not statistically significant. In conclusion, this study showed that beta-endorphin concentrations are increased in COPD patients whether or not they receive oxygen therapy.

Topics: beta-Endorphin; Blood Glucose; Case-Control Studies; Female; Glucagon; Glucose Tolerance Test; Humans; Insulin; Lung Diseases, Obstructive; Male; Middle Aged