Jens Spiesshoefer1,2, Carolin Henke3, Hans Joachim Kabitz4, Jerzy Roch Nofer5,6, Michael Mohr7, Georg Evers7, Jan-Kolia Strecker8, Tobias Brix9, Winfried Johannes Randerath10,11, Simon Herkenrath10,11, Lars Henning Schmidt7, Matthias Boentert3. 1. Respiratory Physiology Laboratory, Department of Neurology with Institute for Translational Neurology, University Hospital Münster, Münster, Germany, jens.spiesshoefer@ukmuenster.de. 2. Institute of Life Sciences, Scuola Superiore Sant'Anna, Pisa, Italy, jens.spiesshoefer@ukmuenster.de. 3. Respiratory Physiology Laboratory, Department of Neurology with Institute for Translational Neurology, University Hospital Münster, Münster, Germany. 4. Department of Pneumology, Cardiology and Intensive Care Medicine, Klinikum Konstanz, Konstanz, Germany. 5. Center for Laboratory Medicine, University Hospital Münster, University of Münster, Münster, Germany. 6. Institute of Clinical Chemistry and Laboratory Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. 7. Department of Medicine A, Hematology, Oncology and Pulmonary Medicine, University Hospital Münster, Münster, Germany. 8. Institute of Life Sciences, Scuola Superiore Sant'Anna, Pisa, Italy. 9. Institute of Medical Informatics, University of Münster, Münster, Germany. 10. Bethanien Hospital gGmbH, Solingen, Germany. 11. Institute for Pneumology at the University of Cologne, Solingen, Germany.
Abstract
BACKGROUND: In lung transplant recipients (LTRs), restrictive ventilation disorder may be present due to respiratory muscle dysfunction that may reduce exercise capacity. This might be mediated by pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). OBJECTIVE: We investigated lung respiratory muscle function as well as circulating pro-inflammatory cytokines and exercise capacity in LTRs. METHODS: Fifteen LTRs (6 female, age 56 ± 14 years, 63 ± 45 months post-transplantation) and 15 healthy controls matched for age, sex, and body mass index underwent spirometry, measurement of mouth occlusion pressures, diaphragm ultrasound, and recording of twitch transdiaphragmatic (twPdi) and gastric pressures (twPgas) following magnetic stimulation of the phrenic nerves and the lower thoracic nerve roots. Exercise capacity was quantified using the 6-min walking distance (6MWD). Plasma IL-6 and TNF-α were measured using enzyme-linked immunosorbent assays. RESULTS: Compared with controls, patients had lower values for forced vital capacity (FVC; 81 ± 30 vs.109 ± 18% predicted, p = 0.01), maximum expiratory pressure (100 ± 21 vs.127 ± 17 cm H2O, p = 0.04), diaphragm thickening ratio (2.2 ± 0.4 vs. 3.0 ± 1.1, p = 0.01), and twPdi (10.4 ± 3.5 vs. 17.6 ± 6.7 cm H2O, p = 0.01). In LTRs, elevation of TNF-α was related to lung function (13 ± 3 vs. 11 ± 2 pg/mL in patients with FVC ≤80 vs. >80% predicted; p < 0.05), and lung function (forced expiratory volume after 1 s) was closely associated with diaphragm thickening ratio (r = 0.81; p < 0.01) and 6MWD (r = 0.63; p = 0.02). CONCLUSION: There is marked restrictive ventilation disorder and respiratory muscle weakness in LTRs, especially inspiratory muscle weakness with diaphragm dysfunction. Lung function impairment relates to elevated levels of circulating TNF-α and diaphragm dysfunction and is associated with exercise intolerance.
BACKGROUND: In lung transplant recipients (LTRs), restrictive ventilation disorder may be present due to respiratory muscle dysfunction that may reduce exercise capacity. This might be mediated by pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). OBJECTIVE: We investigated lung respiratory muscle function as well as circulating pro-inflammatory cytokines and exercise capacity in LTRs. METHODS: Fifteen LTRs (6 female, age 56 ± 14 years, 63 ± 45 months post-transplantation) and 15 healthy controls matched for age, sex, and body mass index underwent spirometry, measurement of mouth occlusion pressures, diaphragm ultrasound, and recording of twitch transdiaphragmatic (twPdi) and gastric pressures (twPgas) following magnetic stimulation of the phrenic nerves and the lower thoracic nerve roots. Exercise capacity was quantified using the 6-min walking distance (6MWD). Plasma IL-6 and TNF-α were measured using enzyme-linked immunosorbent assays. RESULTS: Compared with controls, patients had lower values for forced vital capacity (FVC; 81 ± 30 vs.109 ± 18% predicted, p = 0.01), maximum expiratory pressure (100 ± 21 vs.127 ± 17 cm H2O, p = 0.04), diaphragm thickening ratio (2.2 ± 0.4 vs. 3.0 ± 1.1, p = 0.01), and twPdi (10.4 ± 3.5 vs. 17.6 ± 6.7 cm H2O, p = 0.01). In LTRs, elevation of TNF-α was related to lung function (13 ± 3 vs. 11 ± 2 pg/mL in patients with FVC ≤80 vs. >80% predicted; p < 0.05), and lung function (forced expiratory volume after 1 s) was closely associated with diaphragm thickening ratio (r = 0.81; p < 0.01) and 6MWD (r = 0.63; p = 0.02). CONCLUSION: There is marked restrictive ventilation disorder and respiratory muscle weakness in LTRs, especially inspiratory muscle weakness with diaphragm dysfunction. Lung function impairment relates to elevated levels of circulating TNF-α and diaphragm dysfunction and is associated with exercise intolerance.
Authors: Zaid Patel; Colin K Franz; Ankit Bharat; James M Walter; Lisa F Wolfe; Igor J Koralnik; Swati Deshmukh Journal: J Ultrasound Med Date: 2021-03-27 Impact factor: 2.754
Authors: Fausto Braccioni; Daniele Bottigliengo; Andrea Ermolao; Marco Schiavon; Monica Loy; Maria Rita Marchi; Dario Gregori; Federico Rea; Andrea Vianello Journal: Respir Res Date: 2020-10-15