The function of the hypothalamo-pituitary axis in brain dead patients

Arita, Kazunori; Uozumi, Tohru; Oki, Sadaaki; Kurisu, Kaoru; Ohtani, Minako; Mikami, Takashi

doi:10.1007/bf01476288

Cited by 54 publications

(24 citation statements)

References 54 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These observations are in accordance with histological observations in which the pituitary gland shows varying degrees of edema, hemorrhage and coagulative necrosis. These microscopic changes correlate with previous reports, which suggest persistence of partial cerebral flow in some areas in brain-dead patients [30].…”

Section: Consequences Of Brain Death On the Endocrine Systemsupporting

confidence: 92%

What can be learned from brain-death models?

Pratschke¹,

Neuhaus²,

Tullius³

2005

Transplant Int

View full text Add to dashboard Cite

Summary Brain death of the donor is an important risk factor influencing graft outcome. In addition to its nonspecific effects, it potentiates graft immunogenicity and increases host alloresponsiveness. Thus brain death in addition to other unspecific injuries such as organ procurement, preservation and consequences of ischemia/reperfusion injury, contributes towards the change of an inert organ to an immunological altered graft. Prior to engraftment, brain death initiates a cascade of molecular and cellular events including the release of proinflammatory mediators leading to cellular infiltrates. Those events may affect the incidence of both acute and chronic changes, developing and contributing to reduced graft survival. Consequently, strategies to reduce the immunogenicity or the pro‐inflammatory status of the graft are becoming more attractive and might even help to improve organ quality and graft function.

show abstract

Section: Consequences Of Brain Death On the Endocrine Systemsupporting

confidence: 92%

What can be learned from brain-death models?

Pratschke¹,

Neuhaus²,

Tullius³

2005

Transplant Int

View full text Add to dashboard Cite

show abstract

“…As only 38% to 87% of cadaver organ donors, for instance, develop diabetes insipidus from failure of vasopressin release from the hypothalamus and posterior pituitary gland, it is thought that viable cells in these structures may continue to function as long as 2 wk after death (25). Similarly, cells preserved in the periphery of the anterior pituitary, despite extensive central necrosis, may produce thyroid-stimulating hormone, prolactin, growth hormone, and other factors, as detected in BD patients 1 wk later (6,26).…”

Section: Discussionmentioning

confidence: 99%

Normalization of Brain Death—Induced Injury to Rat Renal Allografts by Recombinant Soluble P-Selectin Glycoprotein Ligand

Gasser¹,

Waaga²,

Holthe³

et al. 2002

Journal of the American Society of Nephrology

View full text Add to dashboard Cite

Abstract. Donor brain death has been considered a significant risk factor for both early and late organ allograft dysfunction. This central injury not only evokes an upsurge of catecholamines with resultant peripheral tissue vasoconstriction and ischemia but also promotes release of hormones and inflammatory mediators that may also affect the organs directly. One of the resultant influences of these events is the rapid upregulation of the acute-phase adhesion molecules, the selectins. These initiate leukocyte adhesion to vascular endothelium and trigger subsequent cellular and molecular changes in the compromised tissues. An established F344 3 LEW rat model of chronic rejection was used to examine (1) whether the initial inflammatory events that develop within kidney allografts from brain-dead donors could be normalized using a recombinant soluble form of P-selectin glycoprotein ligand and (2) whether amelioration of these early changes would alter the inexorable progression of chronic allograft rejection. Untreated living donor controls experienced unrelenting chronic rejection over time. This complex process was accelerated in brain-dead donor kidneys. Treatment with P-selectin glycoprotein ligand prevented the early inflammatory changes in the transplanted organs and their subsequent (200 d) functional and morphologic manifestations, particularly when the soluble ligand was administered both to the donor before organ removal and to the recipient after engraftment. This strategy of using a naturally occurring selectin ligand to prevent donor-associated chronic graft dysfunction may be of special clinical interest in cadaver donor transplantation.The clinical findings that kidneys from living unrelated donors perform as well over the short and long term as those from living related sources and that grafts from both donor groups are invariably superior to those from cadavers have emphasized that antigen-independent events, which include increased donor age and intercurrent disease, the state of brain death, and the period of ischemia, influence the quality of solid organs after transplantation and are important risk factors for their eventual outcome (1,2). Brain death, a central catastrophe unique to the cadaver organ donor, produces profound physiologic and structural derangements in the peripheral tissues of experimental animals both before and after placement in the recipient (3,4). These include massive upregulation of major histocompatibility antigens, adhesion molecules, cytokines, and other acute-phase proteins. Ischemia with systemic vasoconstriction is an important facet of brain death, secondary to the initial burst of catecholamines released into the circulation (5). The early injury and the associated reperfusion after transplantation evoke nonspecific inflammatory changes in the affected organs. However, additional factors may contribute to the peripheral effects of brain injury. Important changes in the dynamics of a series of hormones have been identified (6,7). Because brain death may also influ...

show abstract

“…The heart develops an increased propensity toward arrhythmias, neuroendocrine release increase causes a surge in catecholamines, and hypothalamic hormonal systems continue to function, contributing to a loss of homeostasis. 9,10 These dramatic systemic perturbations have been shown to injure and activate solid organs, including the heart, resulting in an intense inflammatory reaction. 11,12 Several studies with animal models have demonstrated an upregulation in cytokines, chemokines, adhesion molecules, leukocyte activation, and immunoregulatory molecules in transplanted hearts from brain dead donors.…”

Section: Brain Deathmentioning

confidence: 99%

Activation of the endothelium in cardiac allografts

Verrier¹

2004

The Journal of Heart and Lung Transplantation

View full text Add to dashboard Cite

The function of the hypothalamo-pituitary axis in brain dead patients

Cited by 54 publications

References 54 publications

What can be learned from brain-death models?

What can be learned from brain-death models?

Normalization of Brain Death—Induced Injury to Rat Renal Allografts by Recombinant Soluble P-Selectin Glycoprotein Ligand

Activation of the endothelium in cardiac allografts

Contact Info

Product

Resources

About