Functional evidence of reversible ischemic injury immediately after the sympathetic storm associated with experimental brain death

Ryan, Jonathon B.; Hicks, Mark; Cropper, Jonathan R.; Garlick, Sarah; Kesteven, Scott; Wilson, Michael K.; Feneley, Michael P.; Macdonald, Peter S.

doi:10.1016/s1053-2498(02)00558-2

Cited by 51 publications

(33 citation statements)

References 23 publications

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“…Several investigators have demonstrated experimentally that cardiac contractility as assessed by the PRSW relationship deteriorates in untreated animals after brain death (36)(37)(38). The reasons for this decline are likely to be multifactorial.…”

Section: Discussionmentioning

confidence: 99%

“…The reasons for this decline are likely to be multifactorial. The fall in cardiac contractility is biphasic with an initial transient decrease which may be caused by myocardial ischemia (38) or rapid desensitization of the b-adrenergic signalling pathway (39) during the 'autonomic storm'. This is followed by a sustained reduction in contractility which may be due to ongoing catecholamine-induced myocardial ischemia (10, 37), impaired b-adrenergic signaling (39), impaired myocardial metabolism associated with the altered neurohormonal environment after brain death (16,37,40) or upregulation of pro-inflammatory mediators (7,37).…”

Section: Discussionmentioning

confidence: 99%

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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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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

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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“…The catecholamine surge leads to an imbalance between oxygen consumption and supply, resulting in ischemic damage. 26,27 Heart rates of Ͼ200 beats per minute consume high levels of oxygen and, due to inadequate filling time, oxygen circulation is impaired. Immediately after brain death, the maximum heart rate in the group Figure 4.…”

Section: Discussionmentioning

confidence: 99%

Beta-adrenergic Receptor Antagonism Preserves Myocardial Function After Brain Death in a Porcine Model

McLean

Pandalai

Pearl

et al. 2007

The Journal of Heart and Lung Transplantation

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“…It has been recognized that the loss of brain stem function can lead to marked autonomic and endocrine dysfunction that may impact at least on early graft function (53,94,268). Determination of death as complete cessation of cardiorespiratory function [so-called donation after cardiac death (DCD)] was used in early solid-organ cadaveric transplantation (334).…”

Section: Technical Aspects Of Transplantation Donorsmentioning

confidence: 99%

Exercise Limitation Following Transplantation

Williams

McKenna

2012

Comprehensive Physiology

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Organ transplantation is one of the medical miracles or the 20th century. It has the capacity to substantially improve exercise performance and quality of life in patients who are severely limited with chronic organ failure. We focus on the most commonly performed solid‐organ transplants and describe peak exercise performance following recovery from transplantation. Across all of the common transplants, evaluated significant reduction in o 2 peak is seen (typically renal and liver 65%‐80% with heart and/or lung 50%‐60% of predicted). Those with the lowest o 2 peak pretransplant have the lowest o 2 peak posttransplant. Overall very few patients have a o 2 peak in the normal range. Investigation of the cause of the reduction of o 2 peak has identified many factors pre‐ and posttransplant that may contribute. These include organ‐specific factors in the otherwise well‐functioning allograft (e.g., chronotropic incompetence in heart transplantation) as well as allograft dysfunction itself (e.g., chronic lung allograft dysfunction). However, looking across all transplants, a pattern emerges. A low muscle mass with qualitative change in large exercising skeletal muscle groups is seen pretransplant. Many factor posttransplant aggravate these changes or prevent them recovering, especially calcineurin antagonist drugs which are key immunosuppressing agents. This results in the reduction of o 2 peak despite restoration of near normal function of the initially failing organ system. As such organ transplantation has provided an experiment of nature that has focused our attention on an important confounder of chronic organ failure‐skeletal muscle dysfunction. © 2012 American Physiological Society. Compr Physiol 2:1937‐1979, 2012.

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Functional evidence of reversible ischemic injury immediately after the sympathetic storm associated with experimental brain death

Cited by 51 publications

References 23 publications

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

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

Beta-adrenergic Receptor Antagonism Preserves Myocardial Function After Brain Death in a Porcine Model

Exercise Limitation Following Transplantation

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