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Endocrine changes and metabolic responses in a validated canine brain death model

Purpose: Endocrinologic and metabolic changes after brain death (BD) have not yet been investigated in a validated animal model. Therefore, the effects of BD on hormonal and metabolic function were studied in 10 dogs (23 to 31 kg). Methods: BD was induced by intracranial pressure increase and valida...

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Bibliographic Details
Published in:Journal of critical care 1995-06, Vol.10 (2), p.56-63
Main Authors: Bittner, Hartmuth B., Kendall, Simon W.H., Chen, Edward P., Van Trigt, Peter
Format: Article
Language:English
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Summary:Purpose: Endocrinologic and metabolic changes after brain death (BD) have not yet been investigated in a validated animal model. Therefore, the effects of BD on hormonal and metabolic function were studied in 10 dogs (23 to 31 kg). Methods: BD was induced by intracranial pressure increase and validated neuropathologically. Plasma concentrations of pituitary, thyroid, adrenal, and pancreatic hormones were measured pre/post BD. The results are expressed as mean (±SEM). Results: A Cushing reflex and diabetes insipidus occurred after BD. Elevated catecholamine levels were documented after 15 minutes whereas the pituitary gland hormones vasopressin and adrenocorticotrophic horomone (ACTH) decreased significantly after 15 and 45 minutes of BD respectively. Thyroxine, triiodothyronine, and glucagon decreased significantly ( P < .01) from 0.58 ng/mL (±0.05),2.20 μg/dL (±0.15), and 49.7 pg/mL (±9.1) respectively to 0.34 ng/mL (±0.03), 1.14 μg/dL (±1.14), and 6.9 pg/mL (±1.4) respectively 420 minutes after BD. The hematocrit increased significantly after BD and declined toward the end of all experiments. Metabolic acidosis occurred immediately after BD and at the end of the experiments. Conclusions: In a simple, reproducible, and reliable animal model of BD, a catecholamine storm, vasopressin and ACTH cessation, and diabetes insipidus were consistent findings. The decrease in cortisol and vasopressin levels warrant consideration of hormonal therapy.
ISSN:0883-9441
1557-8615
DOI:10.1016/0883-9441(95)90017-9