Brain death and its impact on the donor heart—lessons from animal models

Wilhelm, Markus J.; Pratschke, Johann; Laskowski, Igor; Paz, Dustin; Tilney, Nicholas L.

doi:10.1016/s1053-2498(00)00073-5

Cited by 74 publications

(57 citation statements)

References 29 publications

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“…13,[20][21][22][23] These experiments investigate hemodynamic, neuroendocrine, and immunologic changes during and after brain death. However, brain death and donor care never exceeded 6 hours in brain dead rats.…”

Section: Discussionmentioning

confidence: 99%

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Zhang

Cao²,

Wang³

et al. 2014

Exp Clin Transplant

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Objectives: Experimental animal models of brain death that mimic human conditions may be useful for investigating novel strategies that increase quality and quantity of organs for transplant. Materials and Methods: Brain death was induced by increasing intracranial pressure by inflating an intracranial placed balloon catheter. Brain death was confirmed by flatline electroencephalogram, physical signs of apnea, and absence of brain stem reflexes. Donor management was done after brain death. Intracranial pressure and physiologic variables were continually monitored during 9 hours' follow-up. Results: Ninety percent of brain dead animals showed typical signs of brain death such as diabetes insipidus, hypertensive, and hypotensive periods. Donor care was performed for 9 hours after brain death, and the mean arterial pressure was maintained above 60 mm Hg. Conclusions: We conclude that the rat model of brain death can be performed in a standardized, reproducible, and successful way.

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Section: Discussionmentioning

confidence: 99%

“…Brain death provokes hemodynamic, neuroendocrine, and immunologic changes. [10][11][12][13] To prevent excess variations in blood pressure, inotropic support or manipulation of intracranial balloon volume is issued to maintain normotension in brain dead models. Vasopressors have known adverse events on several organs.…”

Section: Introductionmentioning

confidence: 99%

Untitled

Zhang

Cao²,

Wang³

et al. 2014

Exp Clin Transplant

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“…The success of transplantation is critically dependant upon the quality of the donor organ, which is significantly influenced by the process of donor brain death (6)(7)(8)(9)(10)(11). Reported consequences of brain death include hemodynamic instability and donor organ dysfunction (7,9,10,12,13), rejection of organs for transplantation, and an overall increase in posttransplant complications (6,7,13,14).…”

Section: Introductionmentioning

confidence: 99%

“…A characteristic feature of brain death is the 'sympathetic/autonomic storm' causing extreme hypertension and tachycardia, followed by loss of sympathetic tone and massive vasodilatation leading to hemodynamic instability (13). The substantial increase in endogenous catecholamines that accompanies the 'storm' (15) causes organ ischemia (7,10,13) and increases cardiomyocyte intracellular calcium, which in turn initiates a cascade of events leading to disturbed metabolism, cellular injury and death (7,10,11,16). There is also associated myocardial structural damage (17), impaired ATP production (13,18) and free radical-mediated damage (13).…”

Section: Introductionmentioning

confidence: 99%

The Effects of Hormone Resuscitation on Cardiac Function and Hemodynamics in a Porcine Brain-Dead Organ Donor Model

Hing

Hicks

Garlick

et al. 2007

American Journal of Transplantation

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We compared the effects of hormone resuscitation (HR) with a norepinephrine-based protocol on cardiac function, hemodynamics and need for vasopressor support after brain death in a porcine model. Following brain death induction, animals were treated with norepinephrine and fluids for 3 h. In the following 3 h, they continued on norepinephrine and fluids (control) or received additional HR (triiodothyronine, methylprednisolone, vasopressin, insulin). Data were collected pre-brain death, 3 and 6 h post-brain death. At 6 h, median norepinephrine use was higher in controls (0.563 vs. 0 lg/kg/min; p < 0.005), with 6/8 HR animals weaned off norepinephrine compared with 0/9 controls. Mean arterial pressure was higher in HR animals at 6 h (74 ± 17 vs. 54 ± 14 mmHg; p < 0.05). Cardiac contractility was also significantly higher in HR animals at 6 h (stroke work index 1.777 vs. 1.494). After collection of 6 h data, all animals were placed on the same low dose of norepinephrine. At 6.25 h, HR animals had higher stroke work (3540 ± 1083 vs. 1536 ± 702 mL.mmHg; p < 0.005), stroke volume (37.2 ± 8.2 vs. 21.5 ± 9.8 mL; p < 0.01) and cardiac output (5.8 ± 1.4 vs. 3.2 ± 1.2 L/min; p < 0.005). HR in a porcine model of brain death reduces norepinephrine requirements, and improves hemodynamics and cardiac function. These results support the use of HR in the management of the brain-dead donor.

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“…The endothelial cell is thought to play an important role, since endothelial damage evokes a nonspecific response to injury, resulting in neointimal hyperplasia (7)(8)(9). This injury can occur in the donor as a consequence of incompletely understood brain-death-related mechanisms, such as the catecholamine storm (10,11), following organ procurement during the period of hypoxic hypothermic preservation in hyperosmolar preservation solutions (12)(13)(14)(15) and immediately on retransplantation as a result of neutrophil and free-radical-mediated reperfusion injury (16)(17)(18)(19)(20)(21)(22)(23).…”

Section: Introductionmentioning

confidence: 99%

Cold Storage Preservation and Warm Ischaemic Injury to Isolated Arterial Segments: Endothelial Cell Injury

Neil¹,

Lynch

Hardie

et al. 2002

American Journal of Transplantation

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Injury to endothelial cells is thought to be important to the development of the vascular lesion of chronic rejection. It was the aim of this study to develop a semiquantitative method to assess endothelial injury in arterial grafts and to document the injury produced by cold storage preservation and additional warm ischaemia. Twelve-and 24-h cold preservation of rat aortic segments, together with an additional 1 h of warm ischaemia, were assessed. Electron micrographs of representative endothelial cells were scored for cytoplasmic, nuclear and mitochondrial injury.

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Brain death and its impact on the donor heart—lessons from animal models

Cited by 74 publications

References 29 publications

Untitled

Untitled

The Effects of Hormone Resuscitation on Cardiac Function and Hemodynamics in a Porcine Brain-Dead Organ Donor Model

Cold Storage Preservation and Warm Ischaemic Injury to Isolated Arterial Segments: Endothelial Cell Injury

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