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Juan C Llosa - One of the best experts on this subject based on the ideXlab platform.
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Celsior versus microplegia analysis of myocardial protection in elective aortic valve replacement
The Annals of Thoracic Surgery, 2017Co-Authors: Jose Lopezmenendez, Javier Miguelena, Carmen Luisa Diaz, Francisco Callejo, Juan C Llosa, Carlos Morales, Jacobo SilvaAbstract:Background Previous studies have analyzed the efficacy of crystalloid cardioplegic solutions, but the use of Celsior (Genzyme Corp, Boston, MA) as a crystalloid cardioplegic solution has not been evaluated. Methods In this observational retrospective study, Celsior crystalloid solution was compared with an all-blood continuous myocardial protection (microplegia). The study included all patients who underwent elective aortic valve replacement operations in whom the myocardial protection was Celsior or microplegia. The primary end points were surrogates of myocardial protection and death at 30 days. The secondary end point was the safety analysis of the use of Celsior. Results The study included 631 patients, divided in two groups: 219 (34.7%) with microplegia and 412 (65.3%) with Celsior. Troponin T release accurately predicted postoperative death (area under the receiver operating characteristic curve = 0.85). Troponin T increased with the duration of clamp time, and the adjusted time-related increase was lower in the Celsior group. There were no statistically significant differences in the postoperative use of inotropic medication or intraaortic balloon pump. Adjusted postoperative death was lower in Celsior group (odds ratio, 0.33; 95% confidence interval, 0.15 to 0.76). There were no allergic reactions attributed to Celsior and no unexpected toxicity with the use of Celsior (coagulopathy, renal dysfunction, liver dysfunction, or encephalopathy). Conclusions Isolated crystalloid Celsior may be an optimal and safe myocardial protection strategy in aortic valve replacement operations.
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114. Protección miocárdica con Celsior en cirugía cardíaca compleja
Elsevier, 2012Co-Authors: J. López, C. Morales, C.l. Díaz, Juan C LlosaAbstract:Evaluar la eficacia y seguridad del uso de Celsior en dosis única, como cardioplejía en cirugía cardíaca con clampaje prolongado. Material y métodos: Actualmente se está empleando en nuestro centro Celsior como solución cardiopléjica en cirugía cardíaca estándar. Llevamos a cabo un análisis retrospectivo de todos los pacientes intervenidos desde 2007 con tiempos de clamp prolon-gados (> 75 min), intervenidos de cirugía valvular aislada o mixta. Resultados: Quinientos setenta y cuatro pacientes presentaron tiempos de clampaje superiores a los 75 min, distribuidos en: a) 48,1% dosis única de Celsior; b) 46,5% combinación de Celsior y cardioplejía hemática continua, y c) 5,4% cardioplejía hemática aislada. El tiempo medio de clampaje fue de 103,46 min (desviación estándar [DE] 21,65). A pesar de que los tiempos de clamp fueron significativamente mayores en el grupo de Celsior –a) 106,87 min; b) 101,30 min, y c) 92,06 min; p = 0,012–, no hubo diferencias significativas en niveles de troponina máxima postoperatoria –a) 1,83 mg/l; b) 2,41 mg/l y c) 2,20 mg/l–. El latido espontáneo fue más frecuente en el grupo de hemática, no significativa la diferencia –a) 72,3%; b) 77,7%, y c) 86,7%; p = 0,12. No se encontraron diferencias significativas postoperatorias en uso de aminas, vasopresores, balón de contrapulsación intraaórtica (BCIA), tiempo de ventilación mecánica o empleo de hemofiltración/diálisis. La mortalidad fue: a) 8,9%; b) 9,9%, y c) 16,1%, no significativa la diferencia. Conclusiones: La Celsior como cardioplejía cristaloide aislada en clampajes prolongados facilita la técnica quirúrgica, consiguiendo un campo quirúrgico estable sin sangre, sin comprometer con ello la protección miocárdica
Dobson, Geoffrey P. - One of the best experts on this subject based on the ideXlab platform.
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Early reperfusion with warm, polarizing adenosine–lidocaine cardioplegia improves functional recovery after 6 hours of cold static storage
The American Association for Thoracic Surgery. Published by Mosby Inc., 2011Co-Authors: Rudd, Donna M., Dobson, Geoffrey P.Abstract:ObjectiveRewarming and reanimating the donor heart from cold static storage predisposes the organ to injury and graft dysfunction. Our main aim was to investigate the effects of 5 minutes of continuous rewarming with a normokalemic, oxygenated, polarizing adenosine–lidocaine arrest solution after 6 hours of cold static storage (4°C) in adenosine–lidocaine or Celsior (Genzyme Corp, Cambridge, Mass) solutions.MethodsMale Sprague–Dawley rats (350–450 g, n = 40) were randomly assigned to one of 5 groups: (1) adenosine–lidocaine cold arrest with modified Krebs–Henseleit rewarming, (2) adenosine–lidocaine cold arrest with adenosine–lidocaine rewarming, (3) Celsior cold arrest with Celsior rewarming, (4) Celsior cold arrest with Krebs–Henseleit, and (5) Celsior cold arrest with adenosine–lidocaine arrest rewarming. Hearts were perfused in working mode, arrested (37°C), removed and stored for 6 hours at 4°C, reattached in Langendorff mode, and rewarmed for 5 minutes (37°C). Hearts were switched to working mode, and function was compared with prestorage values. Myocardial oxygen consumption and effluent lactate and pH values were measured during rewarming and recovery.ResultsCold adenosine–lidocaine hearts rewarmed with Krebs–Henseleit recovered 40% aortic flow and 58% coronary flow at 60 minutes of reperfusion. Rewarming with adenosine–lidocaine arrest solution led to significantly higher aortic flow (63%) and coronary flow (77%) at 60 minutes. Cold Celsior hearts rewarmed with Celsior had 9 times higher effluent lactate values with acidosis (pH 6.5) during the last minute of rewarming compared with all groups, and this was associated with early myocardial, vascular, and electrical stunning. At 5 and 10 minutes of recovery, the aortic flow was 1.0 and 8 mL/min, respectively. If cold Celsior hearts were rewarmed with adenosine–lidocaine, they generated 18-fold higher aortic flow and 16-fold higher coronary flow at 5 minutes. At 60 minutes, cold Celsior with Celsior-rewarmed hearts recovered 35% aortic flow and 50% coronary flow compared with 44% aortic flow and 67% coronary flow (P
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Early reperfusion with warm, polarizing adenosine–lidocaine cardioplegia improves functional recovery after 6 hours of cold static storage
Mosby, 2011Co-Authors: Rudd, Donna M., Dobson, Geoffrey P.Abstract:Objective\ud Rewarming and reanimating the donor heart from cold static storage predisposes the organ to injury and graft dysfunction. Our main aim was to investigate the effects of 5 minutes of continuous rewarming with a normokalemic, oxygenated, polarizing adenosine–lidocaine arrest solution after 6 hours of cold static storage (4°C) in adenosine–lidocaine or Celsior (Genzyme Corp, Cambridge, Mass) solutions.\ud \ud Methods\ud Male Sprague–Dawley rats (350–450 g, n = 40) were randomly assigned to one of 5 groups: (1) adenosine–lidocaine cold arrest with modified Krebs–Henseleit rewarming, (2) adenosine–lidocaine cold arrest with adenosine–lidocaine rewarming, (3) Celsior cold arrest with Celsior rewarming, (4) Celsior cold arrest with Krebs–Henseleit, and (5) Celsior cold arrest with adenosine–lidocaine arrest rewarming. Hearts were perfused in working mode, arrested (37°C), removed and stored for 6 hours at 4°C, reattached in Langendorff mode, and rewarmed for 5 minutes (37°C). Hearts were switched to working mode, and function was compared with prestorage values. Myocardial oxygen consumption and effluent lactate and pH values were measured during rewarming and recovery.\ud \ud Results\ud Cold adenosine–lidocaine hearts rewarmed with Krebs–Henseleit recovered 40% aortic flow and 58% coronary flow at 60 minutes of reperfusion. Rewarming with adenosine–lidocaine arrest solution led to significantly higher aortic flow (63%) and coronary flow (77%) at 60 minutes. Cold Celsior hearts rewarmed with Celsior had 9 times higher effluent lactate values with acidosis (pH 6.5) during the last minute of rewarming compared with all groups, and this was associated with early myocardial, vascular, and electrical stunning. At 5 and 10 minutes of recovery, the aortic flow was 1.0 and 8 mL/min, respectively. If cold Celsior hearts were rewarmed with adenosine–lidocaine, they generated 18-fold higher aortic flow and 16-fold higher coronary flow at 5 minutes. At 60 minutes, cold Celsior with Celsior-rewarmed hearts recovered 35% aortic flow and 50% coronary flow compared with 44% aortic flow and 67% coronary flow (P < .05) for Celsior with adenosine–lidocaine–rewarmed hearts. Celsior with Krebs–Henseleit–rewarmed hearts recovered 39% aortic flow and 51% coronary flow and were not significantly different from Celsior-rewarmed hearts. The myocardial oxygen consumption in the last minute of rewarming was 1.6 times higher for cold adenosine–lidocaine hearts rewarmed with adenosine–lidocaine compared with cold Celsior and Celsior hearts (19 vs 12 μmol O2/min/g dry weight) along with low lactate values and no acidosis.\ud \ud Conclusions\ud Rewarming the rat heart after cold static storage in polarizing adenosine–lidocaine arrest solution resulted in significantly higher aortic flow, coronary flow, and cardiac output compared with that seen after Krebs–Henseleit or Celsior rewarming. Rewarming cold Celsior hearts with adenosine–lidocaine solution reduced stunning. Adenosine–lidocaine cardioplegia might offer a new reperfusion strategy after cold static storage
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Eight hours of cold static storage with adenosine and lidocaine (Adenocaine) heart presevation solutions: toward therapeutic suspended animation
'Elsevier BV', 2011Co-Authors: Rudd, Donna M., Dobson, Geoffrey P.Abstract:Objective: Most cardiac preservation solutions provide safe cold ischemic storage times for 4 to 5 hours. Our aim was to investigate the effects of 8 hours of cold static storage (4°C) using 2 normokalemic, polarizing adenosine-lidocaine (Adenocaine; Hibernation Therapeutics Global Ltd, Kilquade, Ireland) solutions and to compare their functional recovery with hearts preserved in gold standard histidine-tryptophan-ketoglutarate (Custodiol-HTK; Essential Pharma, Newtown, Pa) and Celsior (Genzyme, Cambridge, Mass) solutions. Methods: Male Sprague–Dawley rats (350–450 g) were randomly assigned to 1 of 4 groups (n = 8): (1) adenosine-lidocaine cardioplegia with low Ca2+/high Mg2+; (2) 2× adenosine-lidocaine cardioplegia, low Ca2+/high Mg2+, melatonin, and insulin (2× adenosine, lidocaine, melatonin, and insulin); (3) histidine-tryptophan-ketoglutarate solution; or (4) Celsior. Hearts were perfused in working mode, arrested (37°C), removed, stored for 8 hours at 4°C, reattached in Langendorff mode and rewarmed for 5 minutes (37°C), and switched to working mode for 60 minutes. Myocardial oxygen consumption, effluent lactates, and troponin T levels were measured. Results: Hearts preserved for 8 hours in adenosine-lidocaine and 2× adenosine, lidocaine, melatonin, and insulin returned 50% and 76% of aortic flow and 70% and 86% of coronary flow, respectively, at 60 minutes of reperfusion. In contrast, Custodiol-HTK and Celsior hearts returned 2% and 17% of aortic flow and 11% and 48% of coronary flow, respectively, at 60 minutes of reperfusion. Hearts preserved in adenosine-lidocaine and 2× adenosine, lidocaine, melatonin, and insulin returned 90% and 100% of developed pressures and 101% and 104% of heart rate, respectively. Hearts preserved in histidine-tryptophan-ketoglutarate failed to increase systolic pressure greater than 14 mm Hg (11% baseline) and diastolic pressure greater than 10 mm Hg (17% baseline), and recovered only 16% of heart rate. Hearts preserved in Celsior developed 70% of baseline systolic pressures and 86% recovery of heart rate. At 5 minutes of rewarming after cold storage, the myocardial oxygen consumption for hearts preserved in adenosine-lidocaine, 2× adenosine, lidocaine, melatonin, and insulin, Custodiol-HTK, and Celsior was 23.0 ± 5, 20 ±4, 15 ± , and 10 ± 2μmol O2/min/g dry wt, respectively, with corresponding lactate outputs of 1.8 ± 0., 1.5 ± 0.7 2.6 ± 0.7,and 3.2 ± 1.4 μol lactate/min/g dry weight. Troponin T was not detected in the coronary effluent of adenosine-lidocaine or 2× adenosine, lidocaine, melatonin, and insulin hearts, whereas Custodiol-HTK and Celsior hearts had troponin T levels of 0.08 and 0.24 μg/mL, respectively. Conclusions: We report a 78% return of cardiac output, 90% to 100% return of developed pressures, and 101% to 104% return of heart rate after 8 hours of cold static storage using normokalemic, adenosine, lidocaine, melatonin, and insulin preservation solution in the isolated rat heart compared with 55% cardiac output with polarizing adenosine-lidocaine cardioplegia alone, 4% cardiac output with Custodiol-HTK, and 25% cardiac output in Celsior preservation solutions
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Toward a new cold and warm nondepolarizing, normokalemic arrest paradigm for orthotopic heart transplantation
Mosby, 2009Co-Authors: Rudd, Donna M., Dobson, Geoffrey P.Abstract:Objective: Currently, the safe human heart preservation time is limited to around 4 to 5 hours of cold ischemic storage. Longer arrest times can lead to donor heart damage, early graft dysfunction, and chronic rejection. The aim of this study was to examine a new nondepolarizing, normokalemic preservation solution with adenosine and lidocaine for as long as 6 hours of arrest at cold and warmer storage temperatures.\ud \ud Methods: Isolated perfused rat hearts (n = 87) were switched from working to Langendorff (nonworking) mode and arrested at 37°C with 200-µmol/L adenosine and 500-µmol/L lidocaine in Krebs–Henseleit buffer (10-mmol/L glucose, pH 7.7, 37°C) or with Celsior (Sangstat Medical Corp, Fremont, CA). Hearts were removed and placed in static storage at 4°C for 2 and 6 hours or remained on the apparatus and were intermittently flushed at 37°C every 20 minutes for 2 minutes at 68 mm Hg (average arrest temperature 28°–30°C) for 2 and 6 hours. We further investigated the effect of the warmer adenosine–lidocaine solution supplemented with 1- or 5-mmol/L pyruvate.\ud \ud Results: Adenosine–lidocaine solution arrested hearts in 16 ± 2 seconds (n = 32), whereas Celsior did so in 39 ± 4 seconds (n = 23). After 2 hours of cold static storage, there were no functional differences between the adenosine–lidocaine and Celsior groups, with approximately 70% return of cardiac output. In contrast, after 6 hours of 4°C storage, adenosine–lidocaine hearts had significantly higher functional recoveries (68% ± 5% cardiac output) than Celsior hearts (47% ± 14% cardiac output) during 60 minutes of reperfusion. In addition, Celsior hearts took 5 minutes longer to reanimate and showed early reperfusion arrhythmias. At warmer temperatures after 2 hours of arrest, adenosine–lidocaine and Celsior hearts were not significantly different, despite a 43% higher cardiac output in adenosine–lidocaine hearts (80% ± 3% vs 56% ± 12%). After 6 hours, adenosine–lidocaine hearts had recovered 55% ± 3% of prearrest cardiac output, which increased significantly to 75% ± 4% with addition of 1-mmol/L pyruvate. Adenosine–lidocaine with 1-mmol/L pyruvate hearts spontaneously recovered 106% heart rate, 93% to 105% developed pressures, 70% aortic flow, and 81% coronary flow. Coronary vascular resistance increased 1.7- to 1.9-fold during the 6-hour arrest. In contrast, Celsior hearts did not have return of aortic or coronary flow after 6 hours in these warmer conditions.\ud \ud Conclusion: A new nondepolarizing, normokalemic adenosine–lidocaine arrest solution in Krebs–Henseleit buffer with 10-mmol/L glucose was versatile at both 4°C and 28°C to 30°C relative to Celsior, and the addition of 1-mmol/L pyruvate significantly improved cardiac output at warmer arrest temperatures. This new arrest paradigm may be useful in the harvest, storage, and implantation of donor hearts
Geoffrey P Dobson - One of the best experts on this subject based on the ideXlab platform.
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eight hours of cold static storage with adenosine and lidocaine adenocaine heart preservation solutions toward therapeutic suspended animation
The Journal of Thoracic and Cardiovascular Surgery, 2011Co-Authors: Donna Rudd, Geoffrey P DobsonAbstract:Objective Most cardiac preservation solutions provide safe cold ischemic storage times for 4 to 5 hours. Our aim was to investigate the effects of 8 hours of cold static storage (4°C) using 2 normokalemic, polarizing adenosine-lidocaine (Adenocaine; Hibernation Therapeutics Global Ltd, Kilquade, Ireland) solutions and to compare their functional recovery with hearts preserved in gold standard histidine-tryptophan-ketoglutarate (Custodiol-HTK; Essential Pharma, Newtown, Pa) and Celsior (Genzyme, Cambridge, Mass) solutions. Methods Male Sprague–Dawley rats (350–450 g) were randomly assigned to 1 of 4 groups (n = 8): (1) adenosine-lidocaine cardioplegia with low Ca 2+ /high Mg 2+ ; (2) 2× adenosine-lidocaine cardioplegia, low Ca 2+ /high Mg 2+ , melatonin, and insulin (2× adenosine, lidocaine, melatonin, and insulin); (3) histidine-tryptophan-ketoglutarate solution; or (4) Celsior. Hearts were perfused in working mode, arrested (37°C), removed, stored for 8 hours at 4°C, reattached in Langendorff mode and rewarmed for 5 minutes (37°C), and switched to working mode for 60 minutes. Myocardial oxygen consumption, effluent lactates, and troponin T levels were measured. Results Hearts preserved for 8 hours in adenosine-lidocaine and 2× adenosine, lidocaine, melatonin, and insulin returned 50% and 76% of aortic flow and 70% and 86% of coronary flow, respectively, at 60 minutes of reperfusion. In contrast, Custodiol-HTK and Celsior hearts returned 2% and 17% of aortic flow and 11% and 48% of coronary flow, respectively, at 60 minutes of reperfusion. Hearts preserved in adenosine-lidocaine and 2× adenosine, lidocaine, melatonin, and insulin returned 90% and 100% of developed pressures and 101% and 104% of heart rate, respectively. Hearts preserved in histidine-tryptophan-ketoglutarate failed to increase systolic pressure greater than 14 mm Hg (11% baseline) and diastolic pressure greater than 10 mm Hg (17% baseline), and recovered only 16% of heart rate. Hearts preserved in Celsior developed 70% of baseline systolic pressures and 86% recovery of heart rate. At 5 minutes of rewarming after cold storage, the myocardial oxygen consumption for hearts preserved in adenosine-lidocaine, 2× adenosine, lidocaine, melatonin, and insulin, Custodiol-HTK, and Celsior was 23.0 ± 5, 20 ± 4, 15 ± 1, and 10 ± 2 μmol O 2 /min/g dry wt, respectively, with corresponding lactate outputs of 1.8 ± 0.8, 1.5 ± 0.7, 2.6 ± 0.7, and 3.2 ± 1.4 μmol lactate/min/g dry weight. Troponin T was not detected in the coronary effluent of adenosine-lidocaine or 2× adenosine, lidocaine, melatonin, and insulin hearts, whereas Custodiol-HTK and Celsior hearts had troponin T levels of 0.08 and 0.24 μg/mL, respectively. Conclusions We report a 78% return of cardiac output, 90% to 100% return of developed pressures, and 101% to 104% return of heart rate after 8 hours of cold static storage using normokalemic, adenosine, lidocaine, melatonin, and insulin preservation solution in the isolated rat heart compared with 55% cardiac output with polarizing adenosine-lidocaine cardioplegia alone, 4% cardiac output with Custodiol-HTK, and 25% cardiac output in Celsior preservation solutions.
Matthias Ochs - One of the best experts on this subject based on the ideXlab platform.
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Exogenous surfactant application in a rat lung ischemia reperfusion injury model: effects on edema formation and alveolar type II cells
Respiratory Research, 2008Co-Authors: Niels Dreyer, Christian Mühlfeld, Antonia Fehrenbach, Thomas Pech, Sebastian Von Berg, Ragi Nagib, Joachim Richter, Thorsten Wittwer, Thorsten Wahlers, Matthias OchsAbstract:Background Prophylactic exogenous surfactant therapy is a promising way to attenuate the ischemia and reperfusion (I/R) injury associated with lung transplantation and thereby to decrease the clinical occurrence of acute lung injury and acute respiratory distress syndrome. However, there is little information on the mode by which exogenous surfactant attenuates I/R injury of the lung. We hypothesized that exogenous surfactant may act by limiting pulmonary edema formation and by enhancing alveolar type II cell and lamellar body preservation. Therefore, we investigated the effect of exogenous surfactant therapy on the formation of pulmonary edema in different lung compartments and on the ultrastructure of the surfactant producing alveolar epithelial type II cells. Methods Rats were randomly assigned to a control, Celsior (CE) or Celsior + surfactant (CE+S) group (n = 5 each). In both Celsior groups, the lungs were flush-perfused with Celsior and subsequently exposed to 4 h of extracorporeal ischemia at 4°C and 50 min of reperfusion at 37°C. The CE+S group received an intratracheal bolus of a modified natural bovine surfactant at a dosage of 50 mg/kg body weight before flush perfusion. After reperfusion (Celsior groups) or immediately after sacrifice (Control), the lungs were fixed by vascular perfusion and processed for light and electron microscopy. Stereology was used to quantify edematous changes as well as alterations of the alveolar epithelial type II cells. Results Surfactant treatment decreased the intraalveolar edema formation (mean (coefficient of variation): CE: 160 mm^3 (0.61) vs. CE+S: 4 mm^3 (0.75); p < 0.05) and the development of atelectases (CE: 342 mm^3 (0.90) vs. CE+S: 0 mm^3; p < 0.05) but led to a higher degree of peribronchovascular edema (CE: 89 mm^3 (0.39) vs. CE+S: 268 mm^3 (0.43); p < 0.05). Alveolar type II cells were similarly swollen in CE (423 μm^3(0.10)) and CE+S (481 μm^3(0.10)) compared with controls (323 μm^3(0.07); p < 0.05 vs. CE and CE+S). The number of lamellar bodies was increased and the mean lamellar body volume was decreased in both CE groups compared with the control group (p < 0.05). Conclusion Intratracheal surfactant application before I/R significantly reduces the intraalveolar edema formation and development of atelectases but leads to an increased development of peribronchovascular edema. Morphological changes of alveolar type II cells due to I/R are not affected by surfactant treatment. The beneficial effects of exogenous surfactant therapy are related to the intraalveolar activity of the exogenous surfactant.
G Kumarasinghe - One of the best experts on this subject based on the ideXlab platform.
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normothermic ex vivo perfusion provides superior organ preservation and enables viability assessment of hearts from dcd donors
American Journal of Transplantation, 2015Co-Authors: L Gao, G Kumarasinghe, A Doyle, A Iyer, Padmashree Rao, Jonathan R Cropper, C Soto, Andrew DinaleAbstract:The shortage of donors in cardiac transplantation may be alleviated by the use of allografts from donation after circulatory death (DCD) donors. We have previously shown that hearts exposed to 30 min warm ischemic time and then flushed with Celsior supplemented with agents that activate ischemic postconditioning pathways, show complete recovery on a blood-perfused ex vivo working heart apparatus. In this study, these findings were assessed in a porcine orthotopic heart transplant model. DCD hearts were preserved with either normothermic ex vivo perfusion (NEVP) using a clinically approved device, or with standard cold storage (CS) for 4 h. Orthotopic transplantation into recipient animals was subsequently undertaken. Five of six hearts preserved with NEVP demonstrated favorable lactate profiles during NEVP and all five could be weaned off cardiopulmonary bypass posttransplant, compared with 0 of 3 hearts preserved with CS (p < 0.05, Fisher's exact test). In conclusion, DCD hearts flushed with supplemented Celsior solution and preserved with NEVP display viability before and after transplantation. Viability studies of human DCD hearts using NEVP are warranted.
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static cold storage of brain dead donor hearts can pharmacological conditioning overcome primary graft failure
Journal of Heart and Lung Transplantation, 2013Co-Authors: M Hicks, L Gao, Andrew Jabbour, G Kumarasinghe, A Doyle, A Iyer, Peter S MacdonaldAbstract:Purpose Static cold storage of hearts from brain dead donors is still the mainstay in cardiac transplantation. The risk of ischaemia-reperfusion injury (IRI) and primary graft failure (PGF) are significant disadvantages of this method. We found that three ‘conditioning’ agents–Glyceryl trinitrate (G), Erythropoietin€ and Zoniporide (Z), when added to standard preservation solutions, attenuate IRI in rat hearts. We aimed to test their efficacy in hearts from brain dead rats in prolonged cold storage. Methods and Materials Rats were subjected to brain death (BD) by inflation of a subdural embolectomy catheter. Invasive haemodynamic changes are shown in Figure 1 . Cardiac function was assessed on an isolated working heart model (IWHM), then hearts arrested and preserved in Celsior for 1, 3 or 6 hours (n=6 each sub-group). Additional hearts from BD donors were arrested and stored for 3 or 6 hours using Celsior with G+E+Z (n=6 for 3h, 6h) and function re-assessed on an IWHM. Results BD hearts had inferior recovery of cardiac output (CO) cf with shams. Supplementing Celsior with G+E+Z significantly improved CO in BD hearts (p Conclusions G, E & Z that activate ‘conditioning’ pathways significantly improve recovery of BD rat hearts after prolonged static cold storage. This data warrants assessing these strategies clinically. [ figure 2 ]