دورية أكاديمية
Diastolic Cardiomyopathy Secondary to Experimentally Induced Exacerbated Emphysema
| العنوان: | Diastolic Cardiomyopathy Secondary to Experimentally Induced Exacerbated Emphysema |
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| المؤلفون: | Grillet, Pierre-Edouard, Desplanche, Elodie, Wynands, Quentin, Gouzi, Fares, Bideaux, Patrice, Fort, Aurelie, Scheuermann, Valérie, Lacampagne, Alain, Virsolvy, Anne, Thireau, Jérôme, de Tombe, Pieter, Bourdin, Arnaud, Cazorla, Olivier |
| المساهمون: | Physiologie & médecine expérimentale du Cœur et des Muscles U 1046 (PhyMedExp), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université de Montpellier (UM), Centre Hospitalier Régional Universitaire Montpellier (CHRU Montpellier), Hôpital Arnaud de Villeneuve CHRU Montpellier |
| المصدر: | ISSN: 1044-1549. |
| بيانات النشر: | HAL CCSD American Thoracic Society |
| سنة النشر: | 2023 |
| المجموعة: | Université de Montpellier: HAL |
| مصطلحات موضوعية: | elastase, cardiac myofilaments, calcium, chronic obstructive pulmonary disease, heart failure with preserved ejection fraction, [SDV]Life Sciences [q-bio] |
| الوصف: | International audience ; Chronic Obstructive Pulmonary Disease (COPD) is a clinical entity of increasing significance.COPD involves abnormalities of the airways and in emphysema, parenchymal pulmonarydestruction. Cardiovascular disease has emerged as a significant comorbidity to COPD. HeartFailure with preserved Ejection Fraction (HFpEF) appears to be particularly associated withCOPD-Emphysema. Traditional treatments have shown limited efficacy in improving COPDassociated HFpEF. This lack of therapeutic efficacy highlights the need to identify potentialmechanisms that link COPD-Emphysema to HFpEF. Therefore, we aimed to study the delayedcardiac physiological impacts in a rat model with acute exacerbated emphysema. Emphysema wasinduced by 4 weekly 4UI elastase intra-tracheal pulmonary instillations and exacerbation by onefinal additional LPS instillation in male Wistar rats. At 5 weeks following the LPS/elastaseexposure, in-vivo and ex-vivo pulmonary and cardiac measurements were performed. Experimentalexacerbated emphysema resulted in decreased pulmonary function and exercise intolerance.Histological analysis revealed parenchymal pulmonary destruction without signs of inflammationor cardiac fibrosis. In-vivo cardiac functional analysis revealed diastolic dysfunction andtachycardia. Ex-vivo analysis revealed a cellular cardiomyopathy with decreased myofilament Ca2+sensitivity, cross-bridge cycling kinetics and increased adrenergic PKA-dependentphosphorylation of troponin-I. Experimental exacerbated emphysema was associated with exerciseintolerance that appeared to be secondary increased β-adrenergic tone and subsequent cardiacmyofilament dysfunction. A β1-receptor antagonist treatment (bisoprolol) started 24h post ELALPSinstillation prevented in-vivo and ex-vivo diastolic dysfunction. These results suggest that novel treatment strategies targeted to the cardiac myofilament may be beneficial to combatexacerbated emphysema associated HFpEF. |
| نوع الوثيقة: | article in journal/newspaper |
| اللغة: | English |
| العلاقة: | hal-04094438; https://hal.science/hal-04094438Test; https://hal.science/hal-04094438/documentTest; https://hal.science/hal-04094438/file/Red-2022-0382OC.R2_Proof_hi.pdfTest |
| DOI: | 10.1165/rcmb.2022-0382OC |
| الإتاحة: | https://doi.org/10.1165/rcmb.2022-0382OCTest https://hal.science/hal-04094438Test https://hal.science/hal-04094438/documentTest https://hal.science/hal-04094438/file/Red-2022-0382OC.R2_Proof_hi.pdfTest |
| حقوق: | info:eu-repo/semantics/OpenAccess |
| رقم الانضمام: | edsbas.5FE952E8 |
| قاعدة البيانات: | BASE |
| DOI: | 10.1165/rcmb.2022-0382OC |
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