Background: Long-term nocturnal non-invasive mechanical ventilation (NIMV) is an effective treatment for obesity-hypoventilation syndrome (OHS), improving central carbon dioxide (CO2) sensitivity. Leptin might contribute to sustain adequate ventilation in obesity. The aim of the study was to investigate the role of leptin in the OHS pathogenesis looking at its relationship to CO2 sensitivity before and after NIMV in OHS patients. Methods: In six obese patients (3F/3M; aged 6379 yr; BMI 47.074.5 kg/m2) with OHS and without obstructive sleep apnoea–hypopnoea (OSAH) diurnal arterial blood gases, fasting plasma leptin concentration and CO2 chemosensitivity were determined before and after 10.375.6 (range 6–20) months of NIMV. Results: After NIMV improvements were observed in gas exchange (PaO2 from 51.376.7 to 75.0710.3 mmHg, po0.01; PaCO2 from 55.574.8 to 43.771.2 mmHg, po0.01; [HCO3 ] from 33.373.8 to 29.871.7 mmol/l, po0.05) and CO2 chemosensitivity, measured as P0.1/ PetCO2 slope (from 0.0970.07 to 0.1870.07 cmH2O/mmHg, po0.05) and VE/PetCO2 slope (from 0.470.3 to 0.970.5 l/min/mmHg, p¼ 0:07). Plasma leptin increased from 34.5721.1 ng/ml to 50.2722.9 ng/ml (po0.01) after NIMV and changes of the P0.1/ PetCO2 slope correlated with percent changes of plasma leptin (r2 ¼ 0:79, po0.05). Conclusions: These findings suggest a possible role of leptin in the recovery of neuromuscular response to hypercapnia obtained during long-term nocturnal NIMV in OHS patients without OSAH.
Long-term non-invasive ventilation increases chemosensitivity and leptin in obesity-hypoventilation syndrome
Redolfi SPrimo
;
2007-01-01
Abstract
Background: Long-term nocturnal non-invasive mechanical ventilation (NIMV) is an effective treatment for obesity-hypoventilation syndrome (OHS), improving central carbon dioxide (CO2) sensitivity. Leptin might contribute to sustain adequate ventilation in obesity. The aim of the study was to investigate the role of leptin in the OHS pathogenesis looking at its relationship to CO2 sensitivity before and after NIMV in OHS patients. Methods: In six obese patients (3F/3M; aged 6379 yr; BMI 47.074.5 kg/m2) with OHS and without obstructive sleep apnoea–hypopnoea (OSAH) diurnal arterial blood gases, fasting plasma leptin concentration and CO2 chemosensitivity were determined before and after 10.375.6 (range 6–20) months of NIMV. Results: After NIMV improvements were observed in gas exchange (PaO2 from 51.376.7 to 75.0710.3 mmHg, po0.01; PaCO2 from 55.574.8 to 43.771.2 mmHg, po0.01; [HCO3 ] from 33.373.8 to 29.871.7 mmol/l, po0.05) and CO2 chemosensitivity, measured as P0.1/ PetCO2 slope (from 0.0970.07 to 0.1870.07 cmH2O/mmHg, po0.05) and VE/PetCO2 slope (from 0.470.3 to 0.970.5 l/min/mmHg, p¼ 0:07). Plasma leptin increased from 34.5721.1 ng/ml to 50.2722.9 ng/ml (po0.01) after NIMV and changes of the P0.1/ PetCO2 slope correlated with percent changes of plasma leptin (r2 ¼ 0:79, po0.05). Conclusions: These findings suggest a possible role of leptin in the recovery of neuromuscular response to hypercapnia obtained during long-term nocturnal NIMV in OHS patients without OSAH.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.


