Arnoldo Santos1,2,3, Eva Rivas4,5, Roberto Rodríguez-Roisin6,7,8, Marcelo Sánchez9, Jesús Ruiz-Cabello2,3,10, Ebymar Arismendi3,5, José G Venegas11. 1. Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. 2. Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain. 3. CIBER de Enfermedades Respiratorias (CIBERES), Madrid, Spain. 4. Servei d'Anestesiologia, Hospital Clínic, Barcelona, Spain. 5. Institut d'investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and Fundació Clínic per a la Recerca Biomédica (FCRB), Barcelona, Spain. 6. CIBER de Enfermedades Respiratorias (CIBERES), Madrid, Spain. rororo@clinic.ub.es. 7. Institut d'investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and Fundació Clínic per a la Recerca Biomédica (FCRB), Barcelona, Spain. rororo@clinic.ub.es. 8. Servei de Pneumologia, Institut Clínic Respiratori, Hospital Clínic, Barcelona, Spain. rororo@clinic.ub.es. 9. Centre de Diagnòstic per la Imatge (CDI), Hospital Clínic, Barcelona, Spain. 10. Universidad Complutense de Madrid (UCM), Madrid, Spain. 11. Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. Jvenegas@alum.mit.edu.
Abstract
BACKGROUND: Bariatric surgery (BS) in severely obese subjects causes a significant reduction of body weight with lung function improvement. We have shown that abnormalities in pulmonary gas exchange in morbidly obese subjects are substantially improved with BS. These abnormalities were thought to be related to reduced lung volumes as well as to abnormal endothelial function induced by low-grade chronic inflammation linked to perivascular adipose tissue (PVAT). In this study, we used computed tomography (CT) to assess whether BS also caused measurable structural changes in the lung tissue volume (Vtiss) and cross-sectional vessel analysis, hypothesizing that these measures could be related to the previously reported lung functional changes. METHODS: This is a post hoc analysis of a previous reported prospective study. Pulmonary vessels and lung volumes, including Vtiss, were quantified in thoracic CT scans. We compared findings in 12 obese women before and after BS and in 8 healthy lean women. RESULTS: Vtiss was significantly elevated in obese subjects before BS compared to control subjects and systematically reduced after BS (by 8 %); other CT lung volumes or vascular areas were not affected in a consistent manner. No relationship was observed between BS-induced individual changes in Vtiss and pulmonary vessel area. CONCLUSIONS: Vtiss is elevated in morbidly obese subjects, compared to lean individuals of similar body height, and is systematically reduced by BS. These effects do not appear related to vascular changes but may be caused by elevated extravascular lung water, due to low-grade inflammation, and/or hypertrophic PVAT in severe obesity.
BACKGROUND: Bariatric surgery (BS) in severely obese subjects causes a significant reduction of body weight with lung function improvement. We have shown that abnormalities in pulmonary gas exchange in morbidly obese subjects are substantially improved with BS. These abnormalities were thought to be related to reduced lung volumes as well as to abnormal endothelial function induced by low-grade chronic inflammation linked to perivascular adipose tissue (PVAT). In this study, we used computed tomography (CT) to assess whether BS also caused measurable structural changes in the lung tissue volume (Vtiss) and cross-sectional vessel analysis, hypothesizing that these measures could be related to the previously reported lung functional changes. METHODS: This is a post hoc analysis of a previous reported prospective study. Pulmonary vessels and lung volumes, including Vtiss, were quantified in thoracic CT scans. We compared findings in 12 obesewomen before and after BS and in 8 healthy lean women. RESULTS: Vtiss was significantly elevated in obese subjects before BS compared to control subjects and systematically reduced after BS (by 8 %); other CT lung volumes or vascular areas were not affected in a consistent manner. No relationship was observed between BS-induced individual changes in Vtiss and pulmonary vessel area. CONCLUSIONS: Vtiss is elevated in morbidly obese subjects, compared to lean individuals of similar body height, and is systematically reduced by BS. These effects do not appear related to vascular changes but may be caused by elevated extravascular lung water, due to low-grade inflammation, and/or hypertrophic PVAT in severe obesity.
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