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Endocrine changes and metabolic responses in a validated canine brain death model
H B Bittner1, S W Kendall, E P Chen
1Department of General and Cardiothoracic Surgery, Duke University Medical Center, Durham, North Carolina 27710, USA.
Journal of Critical Care
|June 1, 1995
Summary
Brain death in dogs caused a catecholamine storm and decreased pituitary hormones, leading to diabetes insipidus. Hormonal therapy may be needed due to reduced cortisol and vasopressin.
Area of Science:
- Neuroendocrinology
- Metabolic Physiology
Background:
- Endocrinologic and metabolic changes following brain death (BD) lack investigation in validated animal models.
- Understanding these changes is crucial for managing organ donation and transplantation protocols.
Purpose of the Study:
- To investigate the endocrinologic and metabolic effects of brain death (BD) in a validated canine model.
- To assess hormonal and metabolic function changes following induced BD.
Main Methods:
- Brain death (BD) was induced via intracranial pressure elevation and neuropathologically validated in 10 dogs.
- Plasma concentrations of pituitary, thyroid, adrenal, and pancreatic hormones were measured before and after BD induction.
Main Results:
- BD induced a Cushing reflex, diabetes insipidus, and elevated catecholamines within 15 minutes.
- Significant decreases were observed in vasopressin and adrenocorticotrophic hormone (ACTH) levels.
- Thyroxine, triiodothyronine, and glucagon levels significantly decreased post-BD, accompanied by metabolic acidosis and hematocrit changes.
Conclusions:
- A reproducible canine model of BD demonstrated consistent findings of a catecholamine storm, vasopressin and ACTH cessation, and diabetes insipidus.
- The observed decreases in cortisol and vasopressin suggest a potential need for hormonal replacement therapy in BD patients.