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- Barklin, Anne, et al.
(författare)
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Alteration of Neuropeptides in the Lung Tissue Correlates Brain Death-Induced Neurogenic Edema
- 2009
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Ingår i: JOURNAL OF HEART AND LUNG TRANSPLANTATION. - : Elsevier BV. - 1053-2498 .- 1557-3117. ; 28:7, s. 725-732
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Tidskriftsartikel (refereegranskat)abstract
- Background: increased intracranial pressure induces neurogenic pulmonary edema (NPE), potentially explaining why only lungs from less than 20% of brain dead organ donors can be used for transplantation. This study investigated the underlying mechanisms of NPE, focusing on neuropeptides, which potently induce vasoconstriction, vasodilatation, and neurogenic inflammation. Methods: Brain death was induced in 10 pigs by increasing the intracranial pressure. Eight additional pigs served as controls. Neuropeptide Y (NPY), calcitonin gene-related peptide (CGRP), and substance P were analyzed in plasma, bronchoalveolar lavage (BAL) fluid, and homogenized lung tissue 6 hours after brain death. Pulmonary oxygen exchange was estimated using partial pressure of arterial oxygen (Pao(2))/fraction of inspired oxygen (FIO2), and pulmonary edema by wet/dry weight ratio. Results: Brain death induced a decrease in PaO2/FIO2 (P less than 0.001) and increased the wet/dry weight of both apical (p = 0.01) and basal lobes (p = 0.03). NPY and CGRP concentrations were higher in the BAL fluid of brain-dead animals compared with controls (p = 0.02 and p = 0.02) and were positively correlated with the wet/dry weight ratio. NPY content in lung tissue was lower in brain-dead animals compared with controls (p = 0.04) and was negatively correlated with the wet/dry weight ratio. There were no differences in substance P concentrations between the groups. Conclusion: NPY was released from the lung tissue of brain-dead pigs, and its concentration was related to the extent of pulmonary edema. NPY may be one of several crucial mediators of neurogenic pulmonary edema, raising the possibility of treatment with NPY-antagonists to increase the number of available lung donors.
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| 3. |
- Jones, David G, et al.
(författare)
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Permanent pacemaker implantation early and late after heart transplantation : clinical indication, risk factors and prognostic implications
- 2011
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Ingår i: The Journal of Heart and Lung Transplantation. - : Elsevier BV. - 1053-2498 .- 1557-3117. ; 30:11, s. 1257-1265
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND:Permanent pacemaker implantation (PPM) early after cardiac transplantation has been shown not to predict a worse outcome. However, the requirement for pacing late after transplantation and its prognostic implications are not fully known. We describe the clinical indications, risk factors and long-term outcome in patients who required pacing early and late after transplantation.METHODS:The transplant database, medical records and pacing database/records were reviewed for all patients undergoing de novo orthotopic cardiac transplantation (n = 389) at our institution between January 1995 and May 2006.RESULTS:A total of 48 patients (12.3%) received a pacemaker after transplantation. Of these patients, 30 were paced early, pre-hospital discharge (25 ± 19 days post-transplantation), and 18 patients had late pacing (3.0 ± 3.3 years post-transplantation). There were no differences in clinical characteristics, use of anti-arrhythmic drugs or length-of-stay post-transplantation between early and late groups. Early indications for pacing were more often sino-atrial (SA) disease (24 of 30, 80%), whereas atrio-ventricular (AV) disease was more likely to occur later (p = 0.03). Risk factors for PPM included use of biatrial anastomosis (p = 0.001) and donor age (p = 0.002). Prior rejection was a univariate but not multivariate (p = 0.09) predictor of the need for PPM. Development of cardiac allograft vasculopathy was not predictive. There was no significant difference in mortality between late and early PPM patients or between late PPM patients and the non-paced patients who survived transplantation and initial stay.CONCLUSIONS:Patients who required PPM late after orthotopic cardiac transplantation had a prognosis comparable to those paced early and those who did not require PPM. The independent risk factors for PPM were biatrial anastomosis and increasing donor age. SA-nodal dysfunction as an indication for PPM was more prevalent early after transplantation, whereas atrioventricular (AV) disease more commonly presented late. The requirement for pacing late after transplantation was not associated with rejection or cardiac allograft vasculopathy.
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| 5. |
- LoMauro, Antonella, et al.
(författare)
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The impaired diaphragmatic function after bilateral lung transplantation : A multifactorial longitudinal study
- 2020
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Ingår i: The Journal of Heart and Lung Transplantation. - : ELSEVIER SCIENCE INC. - 1053-2498 .- 1557-3117. ; 39:8, s. 795-804
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Lung transplantation is a complex but effective treatment of end-stage pulmonary disease. Among the post-operative complications, phrenic nerve injury, and consequent diaphragmatic dysfunction are known to occur but are hitherto poorly described. We aimed to investigate the effect of lung transplantation on diaphragmatic function with a multimodal approach.METHODS: A total of 30 patients were studied at 4 time points: pre-operatively, at discharge after surgery, and after approximately 6 and subsequently 12 months post surgery. The diaphragmatic function was studied in terms of geometry (assessed by the radius of the diaphragmatic curvature delineated on chest X-ray), weakness (considering changes in forced vital capacity when the patient shifted from upright to supine position), force (maximal pressure during sniff), mobility (excursion of the dome of the diaphragm delineated by ultrasound), contractility (thickening fraction assessed by ultrasound), electrical activity (latency and area of compound muscle action potential during electrical stimulation of phrenic nerve), and kinematics (relative contribution of the abdominal compartment to tidal volume).RESULTS: Despite good clinical recovery (indicated by spirometry and 6 minutes walking test), a reduction of the diaphragmatic function was detected at discharge; it persisted 6 months later to recover fully 1 year after transplantation. Diaphragmatic dysfunction was demonstrated in terms of force, weakness, electrical activity, and kinematics. Our data suggest that the dysfunction was caused by phrenic nerve neurapraxia or moderate axonotmesis, potentially as a consequence of the surgical procedure (i.e., the use of ice and pericardium manipulation).CONCLUSIONS: The occurrence of diaphragmatic dysfunction in patients with a good clinical recovery indicates that the evaluation of diaphragmatic function should be included in the post-operative assessment after lung transplantation.
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