| 1. |
- Barklin, Anne, et al.
(author)
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Alteration of Neuropeptides in the Lung Tissue Correlates Brain Death-Induced Neurogenic Edema
- 2009
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In: JOURNAL OF HEART AND LUNG TRANSPLANTATION. - : Elsevier BV. - 1053-2498 .- 1557-3117. ; 28:7, s. 725-732
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Journal article (peer-reviewed)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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| 2. |
- Iversen, Martin, et al.
(author)
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Cyclosporine C2 Levels Have Impact on Incidence of Rejection in De Novo Lung but Not Heart Transplant Recipients: The NOCTURNE Study
- 2009
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In: Journal of Heart and Lung Transplantation. - : Elsevier BV. - 1053-2498 .- 1557-3117. ; 28:9, s. 919-926
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Conference paper (peer-reviewed)abstract
- Background: Cyclosporine (CsA) absorption varies early after transplantation and can be accurately assessed by the area under the absorption curve (AUC). The 2-hour post-dose (C2) level of CsA in whole blood is reported to be a useful surrogate marker of CsA AUC in kidney and liver transplant monitoring, but should be further explored in thoracic organ recipients. Methods: In a 12-month study we included de novo lung (n = 95) and heart (n = 96) recipients. All participants received cyclosporine (Sandimmun Neoral) monitored by CO and blood was collected for analysis of C2 retrospectively. Abbreviated AUC (AUC(0-4)) was measured at 7 days and 3 months. Primary outcome was C2 relation to the frequency of acute cellular rejection (ACR) needing treatment and possible decline in measured glomerular filtration rate (mGFR). Recipients were divided into lower, middle and upper third C2 groups based on 2-week post-operative values (tertiles T1 to T3). Results: C2 was the most robust substitute for AUC(0-4) in the group of patients studied. For lung, but not heart, recipients there were differences in mean number of ACRs (p = 0.05), incidence of any rejections (p = 0.04), mean number of any rejections (p = 0.001) and time to first rejection (p = 0.03) between T1 and T3. C2 did not predict reduction in mGFR. Conclusions: C2 is a sensitive predictor for ACR in lung, but not heart, recipients, C2 was not predictive of a decline in mGFR. This study suggests that management of lung recipients by C2 may diminish the number of ACRs. J Heart Lung Transplant 2009; 28:919-26. Copyright (C) 2009 by the International Society for Heart and Lung Transplantation.
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| 3. |
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| 4. |
- Selimovic, Nedim, 1960, et al.
(author)
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Assessment of pulmonary vascular resistance by Doppler echocardiography in patients with pulmonary arterial hypertension.
- 2007
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In: The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation. - : Elsevier BV. - 1557-3117. ; 26:9, s. 927-34
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Journal article (peer-reviewed)abstract
- BACKGROUND: Assessment of pulmonary artery pressures, cardiac output (CO) and pulmonary vascular resistance (PVR) is crucial in the management of patients with pulmonary arterial hypertension (PAH). The aim of the present study was to investigate whether Doppler echocardiography can be used to determine PVR in patients with PAH. METHODS: Forty-two patients were included and Doppler echocardiography was performed simultaneously (n = 22) and non-simultaneously (n = 60) with right heart catheterization. The tricuspid regurgitation velocity was used to estimate pulmonary arterial peak systolic and diastolic (PADP) pressures (Bernoulli equation). At the time of pulmonary valve opening, right ventricular pressure equals PADP. The tricuspid regurgitation velocity at the time of pulmonary valve opening was measured by superimposing the time from the QRS to the onset of pulmonary flow on the tricuspid regurgitation velocity envelope. Pulmonary capillary wedge pressure, right atrial pressure and CO were assessed using standard Doppler echocardiography methods. Right heart catheterization was performed using Swan-Ganz catheters and thermodilution for CO determination. RESULTS: The differences (mean +/- SD) between catheter and simultaneous/non-simultaneous Doppler echocardiography were 0.3 +/- 0.8 (p = 0.10)/-0.3 +/- 1.1 (p = 0.06) liter/min for CO, 2.9 +/- 5.1 (p = 0.02)/-1.2 +/- 7.4 (p = 0.2) mm Hg for the transpulmonary gradient (TPG) and 0.3 +/- 2.1 (p = 0.65)/0.8 +/- 2.4 (p = 0.02) Wood unit for PVR. The correlation coefficients between catheter and simultaneous/non-simultaneous Doppler echocardiography were 0.86/0.75 for CO, 0.92/0.90 for TPG and 0.93/0.92 for PVR. CONCLUSIONS: A comprehensive hemodynamic assessment that includes CO, TPG and PVR can be provided by Doppler echocardiography in patients with severe pulmonary hypertension.
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| 5. |
- Selimovic, Nedim, 1960, et al.
(author)
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Endothelin-1 across the lung circulation in patients with pulmonary arterial hypertension and influence of epoprostenol infusion.
- 2009
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In: The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation. - : Elsevier BV. - 1557-3117. ; 28:8, s. 808-14
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Journal article (peer-reviewed)abstract
- BACKGROUND: The endothelin-1 (ET-1) system plays a pathophysiologic role in patients with pulmonary arterial hypertension (PAH). Results from previous studies assessing the transpulmonary gradient of ET-1 have been inconsistent. The influence of an intravenous epoprostenol infusion on the transpulmonary ET-1 gradient is unknown. METHODS: In a prospective investigation, serum concentrations of ET-1 were measured in 39 consecutive patients (31 women; mean age, 20-77 years) with pulmonary hypertension (33 with PAH) and compared with 20 controls. The effect of intravenous epoprostenol administration on the transpulmonary gradient of ET-1 was analyzed in 13 patients with pulmonary hypertension. Blood samples were taken simultaneously from the pulmonary artery and radial artery. RESULTS: The serum levels of ET-1 were significantly higher in the arterial (3.9 +/- 1.28 vs 2.53 +/- 0.24 pg/ml, p < 0.001) and mixed venous blood samples (3.9 +/- 1.21 vs 2.52 +/- 0.29 pg/ml, p < 0.001) in patients with pulmonary hypertension than in controls. The arterial/venous ratio of ET-1 in patients (1.0 +/- 0.1) and in the control group (1.0 +/- 0.05) was similar (p = 0.79). During intravenous epoprostenol infusion, there were no changes in the mean transpulmonary ET-1 gradient (0.98 +/- 0.07 vs 0.96 +/- 0.09, p = 0.52), despite significant hemodynamic changes. CONCLUSION: The ET-1 radial artery/pulmonary artery ratio of unity indicates a balanced release and clearance of ET-1 across the lung circulation in controls and in patients with different forms of pulmonary hypertension. ET-1 levels across the pulmonary circulation did not change during epoprostenol infusion.
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| 6. |
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| 7. |
- Tjang, Yanto Sandy, et al.
(author)
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Risk factor analysis in pediatric heart transplantation.
- 2008
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In: The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation. - : Elsevier BV. - 1557-3117. ; 27:4, s. 408-15
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Journal article (peer-reviewed)abstract
- BACKGROUND: Steady assessment of risk factors will enable identification of patients at higher risk for post-transplant death, and may thus improve organ utilization and outcomes. In this study we aimed to identify the risk factors of mortality in pediatric heart transplantation. METHODS: Between November 1989 and February 2004, there were 116 orthotopic heart transplantations performed in patients <18 years of age at our institution. RESULTS: The 30-day mortality risk was 12% (dilated cardiomyopathy 7%, congenital heart disease 26%; univariate analysis: p = 0.023). The main cause of 30-day mortality was primary graft failure (36%). The late mortality rate was 31 per 1,000 person-years. The main causes of late mortality were acute rejection (44%) and cardiac allograft vasculopathy (26%). The 1-, 5-, 10- and 15-year survival rates were 85%, 77%, 65% and 53%, respectively. Male donor (odds ratio [OR] 6.33, 95% confidence interval [CI] 1.11 to 36.01) and cardiopulmonary bypass >210 minutes (OR 43.05, 95% CI 1.11 to 1,669) were risk factors for 30-day mortality. Risk factors for 1- and 5-year mortality were body weight ratio <0.8 (OR 40.36, 95% CI 3.04 to 536.47) and male donor (OR 3.36, 95% CI 1.05 to 10.75), respectively. Recipient age <1 year (OR 64.65, 95% CI 1.69 to 2,466.77) and donor-recipient body surface area mismatch of <0.9 (OR 10.58, 95% CI 1.03 to 108.25) were risk factors for 10-year mortality. CONCLUSIONS: Pediatric heart transplantation can be performed with an expectation of excellent results. Certain risk factors suggest poorer outcomes.
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| 8. |
- Wierup, P, et al.
(author)
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Lung edema formation during cold perfusion: Important differences between rat and porcine lung
- 2005
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In: The Journal of Heart and Lung Transplantation. - : Elsevier BV. - 1557-3117 .- 1053-2498. ; 24:4, s. 379-385
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Journal article (peer-reviewed)abstract
- Background: The aim of this study was to investigate the effect of different perfusion pressures on edema formation during cold flush perfusion with the 2 most commonly used preservation solutions in clinical lung transplantation: Euro-Collins and Perfadex solutions. Methods: Isolated rat and porcine lungs were perfused for 3 minutes at 4 degrees C to 8 degrees C at a pressure of either 10, 15 or 20 mm, Hg. Weight gain was recorded continuously. Weight gain per minute was calculated after the first phase of rapid weight gain was completed. Results: In the rat model, perfusion pressure of 10 mm Hg resulted in a macro- and microscopically apparent edema, irrespective of the type of preservation solution. Perfusion pressures of 10, 15 and 20 nun Hg gave weight gains of 100%, 150% and 350%, respectively, after 3 minutes of perfusion. The corresponding weight gain per minute was 18%, 31% and 84% of the initial weight. There were no statistically significant differences in weight gain between the different solutions at equal perfusion pressure. In the porcine model the flow was extremely low at 10 mm Hg and no weight gain was registered, whereas the weight gain per minute at 15 and 20 mm Hg was 1.0% and 2.1% of the initial weight. Conclusions: In porcine lungs, cold perfusion at 20 mm Hg gives minimal edema formation, whereas in rat lungs the edema formation is deleterious, irrespective of the solution used.
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| 9. |
- Williams, JJ, et al.
(author)
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Excessive weight gain in cardiac transplant recipients
- 2006
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In: The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation. - : Elsevier BV. - 1557-3117. ; 25:1, s. 36-41
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Journal article (peer-reviewed)
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