Anoxia and Brain Potentials

Sugar, Oscar; Gerard, R. W.

doi:10.1152/jn.1938.1.6.558

Cited by 220 publications

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“…Our result was consistent with that of Przybylski (1972), who observed cortical and subcortical EEG and ECG of the rabbit treated with hypoxic mixture of oxygen in nitrogen. It was also consistent in some parts with the findings of acute asphyxial death reported by Sugar and Gerard (1938) and Fujita et al (1969), although the process of drowning in our experiments was markedly prolonged. Typical patterns of the 3rd stage were struggle for expectoration of aspirated water and appearance of bradycardia in ECG in response to the hypoxemia as Katzin and Rubinstein (1974) reported.…”

Section: Discussionsupporting

confidence: 94%

Electrophysiological Studies on Slowly Induced Sea and Fresh Water Drowning in Rabbits

Fujimura

Kômura

Furuno

et al. 1979

Tohoku J. Exp. Med.

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-255 -Surface and deep electroencephalograms , electrocardiogram and behavior of 10 male rabbits were studied by infusing fresh water or sea water slowly at a speed of 0.5-2.0 ml/min, by means of a dripping apparatus, into the canulated trachea until the death of the animals.From the behavior of the animal and EEG and ECG findings, the course was divided into 4 stages. The 1st, alert stage; 2nd, adapted or calm stage; 3rd, dyspnea stage; and 4th, covering from the agonal spasm to ECG silence. The course of this drowning death was quite different from that due to a large amount of water aspirated within a short period. The volume of fresh water needed to kill the animals was 7 times larger than that of the sea water in this method, and the latter was less than half of the volume of sea water necessary for the death due to short period aspira tion. The mechanism of death seems to be slow and prolonged asphyxia and, among the terminal events in fresh water drowning, there might occur marked pulmonary hypertension that results in a high degree of lung edema.In the ECG at terminal stage, final bradycardia (84.4% of normal pulse rate) at around the time of surface EEG disappearance, and final tachycardia (142.7% of normal pulse rate) about 120 sec later than final bradycardia and 40 min later than deep EEG disappearance were observed consistently. After clinical signs of death ECG still continued to beat slowly for 1-2 hr.slowly induced sea and fresh water drowning; permanent electrode; EEG; ECG Since the first heart transplantation was performed in 1967 in our country, the donor-problem has been widely discussed all over Japan, not only from the medical but also from the ethical and moral aspects. One of the authors, as a surgeon, has experienced an operative death case in which continuous ECG tracing was taken for more than one hr after the clinical signs of death. But the courses of events around the time of death of living creatures were not clearly documented so as to be readily applied for the resuscitation and/or organ transplantation etc. by any physicians or surgeons.

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Section: Discussionsupporting

confidence: 94%

Electrophysiological Studies on Slowly Induced Sea and Fresh Water Drowning in Rabbits

Fujimura

Kômura

Furuno

et al. 1979

Tohoku J. Exp. Med.

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“…Morphologic and physiologic responses to injuries and asphyxia in reptiles, birds, fish, amphibians, or quadrupedal mammals may manifest differently from those described as characteristic in people. Anatomic variations in blood supply to the brain 29,49,79,122,135 affect the degree and duration of physiological responses of animals compared to people. 13 In 1897, Brouardel 18 stated ''que la resistance des animaux aux divers genres d'asphyxie est plus grande que celle de l'homme'' (''the resistance of animals to various kinds of asphyxia is greater than that of man'').…”

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Nondrowning Asphyxia in Veterinary Forensic Pathology

McEwen

2016

Vet Pathol

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Asphyxia in a forensic context refers to death by rapid cerebral anoxia or hypoxia due to accidental or nonaccidental injury. Death due to nondrowning asphyxia can occur with strangulation, suffocation, and mechanical asphyxia, each of which is categorized based on the mechanism of injury. Individuals dying due to various types of asphyxia may or may not have lesions, and even those lesions that are present may be due to other causes. The interpretation or opinion that death was due to asphyxia requires definitive and compelling evidence from the postmortem examination, death scene, and/or history. Beyond the postmortem examination, pathologists may be faced with questions of forensic importance that revolve around the behavioral and physiological responses in animals subjected to strangulation, suffocation, or mechanical asphyxia to determine if the animal suffered. While there is no prescriptive answer to these questions, it is apparent that, because of physiological and anatomical differences between humans and animals, for some mechanisms of asphyxia, consciousness is maintained for longer periods and the onset of death is later in animals than that described for people. Veterinary pathologists must be cognizant that direct extrapolation from the medical forensic literature to animals may be incorrect. This article reviews the terminology, classification, mechanisms, and lesions associated with asphyxial deaths in companion animals and highlights significant comparative differences of the response to various types of asphyxia in animals and people.

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“…In fact, a study by McHugh et al (2008) found that both the ventral and dorsal hippocampus is important in cost-benefit decision making. Of particular interest is the fact that hippocampal pyramidal cells (particularly those housed in area CA1) are extremely sensitive to oxygen deprivation (Krnjevic, 1999) and are among the first to arrest function during ischemic insults (Sugar & Gerard, 1938).…”

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confidence: 99%

A Predictive Model of Cognitive Performance Under Acceleration Stress

McKinley

2010

Advances in Human Factors and Ergonomics Series

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A Predictive Model of Cognitive Performance under Acceleration StressExtreme acceleration maneuvers encountered in modern agile fighter aircraft can wreak havoc on human physiology thereby significantly influencing cognitive task performance. Increased acceleration causes a shift in local arterial blood pressure and profusion causing declines in regional cerebral oxygen saturation. As oxygen content continues to decline, activity of high order cortical tissue reduces to ensure sufficient metabolic resources are available for critical life-sustaining autonomic functions.Consequently, cognitive abilities reliant on these affected areas suffer significant performance degradations.This goal of this effort was to develop and validate a model capable of predicting human cognitive performance under acceleration stress. An Air Force program entitled, "Human Information Processing in Dynamic Environments (HIPDE)" evaluated cognitive performance across twelve tasks under various levels of acceleration stress.Data sets from this program were leveraged for model development and validation.Development began with creation of a proportional control cardiovascular model that produced predictions of several hemodynamic parameters including eye-level blood pressure. The relationship between eye-level blood pressure and regional cerebral oxygen saturation (rSO 2 ) was defined and validated with objective data from two different HIPDE experiments. An algorithm was derived to relate changes in rSO 2 within specific brain structures to performance on cognitive tasks that require engagement of iv different brain areas. Data from two acceleration profiles (3 and 7 G z ) in the Motion Inference experiment were used in algorithm development while the data from the remaining two profiles (5 and 7 G z SACM) verified model predictions. Data from the "precision timing" experiment were then used to validate the model predicting cognitive performance on the precision timing task as a function of G z profile. Agreement between the measured and predicted values were defined as a correlation coefficient close to 1, yet complex factor in overall system design. Moreover, many find it convenient to develop the mechanical system separately from the HO and then rectify the interface between the two as the system is being prepared for production. One of the central issues contributing to this ill-advised strategy is the inability of the designer to easily change the inherent characteristics of the human entity. Should a material used in the "skin" of an aircraft react inappropriately to extreme temperature changes, the material can be replaced with an alternative material with properties that allow it to remain inert and invariable with respect to temperature. However, the human element cannot be replaced with a stronger, faster or lighter component. The HO performance characteristics can only be augmented to a limited extent with modern technology, training, and procedures.However, even with the assistance of such technology aids, the HO often reac...

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Anoxia and Brain Potentials

Cited by 220 publications

References 0 publications

Electrophysiological Studies on Slowly Induced Sea and Fresh Water Drowning in Rabbits

Electrophysiological Studies on Slowly Induced Sea and Fresh Water Drowning in Rabbits

Nondrowning Asphyxia in Veterinary Forensic Pathology

A Predictive Model of Cognitive Performance Under Acceleration Stress

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