A Simplified Organ Donor Model Produced by Permanent Complete Central Nervous System Ischemia in Dogs
Thomas S. Huber,Louis G. D'Alecy +1 more
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TLDR
A canine model of complete brain death is developed by infusing saline into the subdural space and elevating intracranial pressure above systolic arterial pressure and it should facilitate the investigation of the mechanisms leading to somatic death in the brain-dead state and ultimately lead to improved clinical supports.About:
This article is published in Journal of Critical Care.The article was published on 1991-03-01 and is currently open access. It has received 7 citations till now. The article focuses on the topics: Cushing reflex & Intracranial pressure.read more
Citations
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Journal ArticleDOI
Hormonal and hemodynamic changes in a validated animal model of brain death
TL;DR: In a validated animal model of brain death, significant decreases in the circulating concentrations of stress hormones, as well as hemodynamic instability, occurred after brain death.
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Myocardial β-Adrenergic Receptor Function and High-Energy Phosphates in Brain Death– Related Cardiac Dysfunction
Hartmuth B. Bittner,Edward P. Chen,Carmelo A. Milano,Simon W.H. Kendall,Robert B. Jennings,David C. Sabiston,Peter Van Trigt +6 more
TL;DR: The loss of ventricular function after BD was more prominent in the right ventricle and may contribute to early postoperative RV failure in the recipient and occur despite BAR system upregulation after BD.
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Endocrine changes and metabolic responses in a validated canine brain death model.
TL;DR: In a simple, reproducible, and reliable animal model of BD, a catecholamine storm, vasopressin and ACTH cessation, and diabetes insipidus were consistent findings, and the decrease in cortisol and vasoppressin levels warrant consideration of hormonal therapy.
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Hormonal Profiles in a Canine Model of the Brain-Dead Organ Donor
Thomas S. Huber,Thomas S. Huber,Ray Nachreiner,Ray Nachreiner,Louis G. D'Alecy,Louis G. D'Alecy +5 more
TL;DR: The inability of the BD group to increase plasma CORT, NE, and EPI may contribute to the hemodynamic deterioration and eventual somatic death.
References
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Hemodynamic and metabolic responses to hormonal therapy in brain-dead potential organ donors.
TL;DR: An evaluation of the beneficial effects of hormonal therapy, consisting of T3 2 micrograms, cortisol 100 mg, and insulin 20 units, administered at hourly intervals intravenously, was assessed in brain-dead patients referred for organ donation, resulting in a significant improvement of cardiovascular status.
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Interaction of Vasopressin and the Baroreceptor Reflex System in the Regulation of Arterial Blood Pressure in the Dog
TL;DR: Decapitated, spinal, anesthetized dogs maintained with a small continuous infusion of norepinephrine exhibited the greatest sensitivity to vasopressin; the threshold dose for a pressor response was similar to that in conscious baroreceptor-denervated dogs, but pressor sensitivity at physiological dose levels was increased nearly 8, 000-fold.
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Change from aerobic to anaerobic metabolism after brain death, and reversal following triiodothyronine therapy.
TL;DR: It is suggested that T3 should be adminstered to all brain-dead potential ortgan donors to correct and maintain a more physiologic metabolic status and thus to improve oragan function.
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Cerebral metabolic state following complete compression ischemia
TL;DR: Recovery of cerebral metabolism after total ischemia was studied in rats by measurements of brain tissue concentrations of carbohydrate substrates, amino acids and organic phosphates at various periods following an increase in the intracranial CSF pressure to values exceeding the mean arterial blood pressure.
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Prevention of myocardial injury during brain death by total cardiac sympathectomy in the Chacma baboon
TL;DR: It is suggested that myocardial damage occurring during the process of dying may be related to endogenous catecholamine release (possibly resulting in increased calcium uptake by the myocardials), inducing various forms of myocyte necrosis, which may result in early failure in a donor heart following cardiac transplantation.