Carbon Monoxide Asphyxia Research Articles

Effects of stunning methods on pre rigor changes in rainbow trout (Oncorhynchus mykiss) reared at two different temperatures

The effects of two stunning methods (carbon monoxide asphyxia, CO, and electroshock, E) on blood plasma parameters, rigor index, fillet pH and shape changes, ATP breakdown and Adenylate Energy Charge (AEC) in muscle immediately post mortem were investigated in rainbow trout (Oncorhynchus mykiss) kept in tanks containing water set at 8 °C or 12 °C. Both the methods here adopted induced a stress-response which, however, was not able to affect the rigor mortis development and fillet pH. The fillets from the E group showed the strongest length contraction and width increase at 48 h post mortem. The CO stunning method exhibited the highest levels of both ATP and AEC in the muscle immediately after death, equal to 2.28 µmol/g and 0.83, respectively, while 1.12 µmol/g and 0.64 values were found in the E group. In addition, we found that the water temperature might interact with the stunning method and minimise the stress response. In the present trial, the most suitable use of the CO stunning method would be coupled with 12 °C of rearing water temperature to better preserve ATP and AEC in muscles. Highlights CO stunning preserves ATP and AEC in trout muscle better than electrical stunning Water temperature might interact with the stunning and minimise the stress response CO stunning is suggested to be coupled with 12 °C of water temperature Electricity should be avoided at 8 °C of water temperature

Effects of stunning/slaughtering methods in rainbow trout (Oncorhynchus mykiss) from death until rigor mortis resolution

The effects of stunning/slaughtering methods (carbon monoxide asphyxia, CO; electroshock, E; asphyxia in the air, A) were studied in rainbow trout kept in freshwater at 12°C. The fish were analysed for blood parameters, rigor mortis evolution, fillets shape changes over 48h, and ATP depletion and Adenylate Energy Charge (AEC) in muscle immediately after death. Treatment A was most stressful giving the lowest pH values during rigor evolution, the highest concentration of lactate (6.31mM) in plasma and the lowest AEC values in the muscle.None of the three-stunning/slaughtering methods affected perimeter, length and height of the fillets, with exception for the area at 24h and 48h post mortem, which was significantly reduced by CO treatment (CO<A<E). Globally, CO and E treatments showed the highest ability in preserving muscle energy immediately after death, whereas treatment E resulted the most suitable method for slaughtering, based on blood and muscle indicators. Statements of relevance1.The application of CO as slaughtering/killing method on rainbow trout, focusing on the effects produced in the pattern of some analytical parameters during the first period post mortem2.The use of carbon monoxide for killing fish has been only recently experimented and only in Atlantic salmon.3.Improve the knowledge about the use of CO, due the scarcity of information in scientific literature

Twenty-nine years after carbon monoxide intoxication

Carbon monoxide (CO) is a worldwide environmental toxin and a leading cause of deliberate or accidental poisoning. There is an extensive literature devoted to the clinical features and treatment of those victims who have survived acute CO poisoning for a short length of time. The long-term sequelae of non-fatal poisoning have received scanty references, and the prospects for the long-lasting survivors of acute CO intoxication are less clear. Literature review uncovered reports of only three patients who were followed for a considerable period of time. We present a case of CO poisoning with progressive neurological and psychological deterioration that began 17 years after recovery from a severe, accidental CO asphyxia. The patient was examined in the neurology out patient clinic 29 years after the initial CO intoxication. We believe the unique status of this patient, her similarity to one other case in the literature and the circumstances allowing correlation of the clinical picture to the CO poisoning warrants emphasis.

Carbon Monoxide: The Unnoticed Poison of the 21 st Century

Accessible online at: www.karger.com/journals/ibe Carbon monoxide is the most ancient of poisons: as old as the discovery of fire itself. However, poisoning by it was probably of no great significance until the general use of coal as a domestic fuel had became widespread and consequent upon that the use of town gas made from coal or oil which was distributed to industry and to homes. A third development was, of course, the internal combustion engine. In this volume we are not concerned with carbon monoxide poisoning in the past rather we are concerned that it is still with us today. We know a lot about carbon monoxide and how dangerous it is and we should, by now, have developed strategies to avoid the danger. Unfortunately the lessons have not been learnt as several of the papers in this issue relate. Probably the best starting point for a study of carbon monoxide poisoning today is the work of Claude Bernard, who opened a modern history of the condition in his lectures on the action of poisons [1]. Bernard devoted a lot of attention to carbon monoxide. He showed that blood saturated with the gas was no longer able to take up oxygen and he attributed its poisonous effects to this action. By preventing the combination of oxygen with haemoglobin carbon monoxide is the perfect asphyxiant. Also, since the combination with carbon monoxide is so much more stable than that made with oxygen and the reaction takes place more readily the gas in a very effective way prevents the process of respiration. In fact, the affinity of haemoglobin for carbon monoxide is some 240 times that for oxygen [2]. A simple chemical reaction that takes place as readily in the body as it does in the testtube. Experiments suggest that this formation of carboxyhaemoglobin is the main, possibly the only, important, biochemical event of carbon monoxide poisoning. Insects without haemoglobin, such as cockroaches, have survived for weeks breathing an atmosphere of 80% carbon monoxide and 20% oxygen. To them the gas is as inert as nitrogen. Even an animal as large as a mouse can survive with its blood fully saturated with carbon monoxide if it is breathing hyperbaric oxygen because, through simple solution, sufficient oxygen for life dissolves in the blood. Larger animals would not be so lucky. The use of oxygen in the treatment of carbon monoxide asphyxia is not modern medicine. It can be traced back to the work of Claude Bernard noted above and when reading it we should remember that oxygen had only been discovered less than 100 years before in 1772 by Scheele. Bernard did not have the advantage of purified gas conveniently delivered in a metal cylinder. He had to prepare the element and store it in a bladder or a gas jar. Not an easy task. Since then, and with oxygen more readily available, experience both in the laboratory and in the field has amply demonstrated the beneficial effect of inhaling oxygen in both mild and severe carbon monoxide poisoning. It is long proven that recovery from dangerous asphyxia as well as alleviation of the headaches and other symptoms of less severe poisoning is substantially promoted when oxygen is given. If an individual is poisoned by carbon monoxide then to maintain life the remaining available haemoglobin in their blood will have to be saturated with oxygen when the blood passes through the lungs. To ensure complete saturation it is necessary to increase the concentration of oxygen breathed from the

Carbon-Monoxide Asphyxia with Visual Sequelae : With Report of a Case

Carbon-Monoxide Asphyxia with Visual Sequelae : With Report of a Case

Gangrene of Lower Extremity Following Carbon Monoxide Asphyxia

Gangrene of Lower Extremity Following Carbon Monoxide Asphyxia

Blood Sugar, Insulin, and Dextrose Tolerance in Albino Rat Treated with Carbon Monoxide

Conclusions1. Acute carbon monoxide asphyxia raises the blood sugar in direct proportion to the percentage of COHb induced. 2. Repeated exposure to carbon monoxide seems not to change the insulin tolerance significantly but to reduce the dextrose tolerance below the limits of normal variation. It reduces the fasting blood sugar 6-8 mg below that of untreated litter mates.

Adventures in Respiration: Modes of Asphyxiation and Methods of Resuscitation.

In this interesting book the author traces the historic milestones leading to the present understanding of the physiology of respiration and discusses the value and rationale of using carbon dioxide in the treatment of various asphyxial states. Arrangement of the subject matter in narrative form, as an adventure of the author in research over a period of years, endows facts and theories with charm and personal interest. The first part of the book is devoted to a consideration of shock, the control of breathing and blood alkali and the "fallacy of asphyxial acidosis," in which discussion the conception of "acarbia" as induced by "hyperpnein" is suggested as a substitute for the theory of "acidosis" induced by lactic or other acid. There are several chapters dealing with the physiologic basis of mountain sickness and acclimatization, carbon monoxide asphyxia and asphyxia of the newborn. The therapeutic value and methods of administration of

Food Intake and Gastro-Intestinal Motility in the Albino Rat During Chronic CO Asphyxia

ConclusionsChronic carbon monoxide asphyxia decreases food Intake and inhibits gastro-intestinal peristalsis, significantly.

Veröffentlichungen aus der Gewerbe- und Konstitutionspathologie

This study of motor traffic and public health and the question whether there are chronic ill effects from exhaust gas is based on observations chiefly on animals exposed to volatilized German motor fuel (benzine) and the exhaust from motors consuming that fuel. German motor fuel generally consists not merely of gasoline from petroleum but contains also considerable amounts of coal distillate; and coal distillate is rich in benzene and related substances. This study is accordingly concerned less with carbon monoxide asphyxia than with benzene poisoning. In the air of streets the author finds that no considerable hazard to health arises either from carbon monoxide or from benzene. Nor is exhaust gas responsible, according to the author, for the increasing occurrence of cancer of the bronchi. Exhaust gas in such dilution as occurs outdoors causes no injury to the lungs. Experiments are, however, reported which afford evidence that the blood-forming organs

METHYLENE BLUE: A SYNERGIST, NOT AN ANTIDOTE, FOR CARBON MONOXIDE

Methylene blue (methylthionine chloride U. S. P.) has recently been much in the lay press, not only as an antidote for cyanide, which it is, but also for carbon monoxide, which it is not. P. J. Hanzlik 1 has reviewed the evidence that this substance is an antidote to cyanide. As he points out, the antagonistic property of methylene blue for cyanide was demonstrated experimentally as early as 1926 and has been confirmed by more recent work. On the other hand, the alleged antagonism between methylene blue and carbon monoxide has no valid support. The theoretical basis of the claim for an antidotal action is derived from the brilliant investigations of Warburg; 2 but Warburg's observations on isolated tissues have no real bearing on carbon monoxide asphyxia in man. The experiments of Matilda M. Brooks 3 on animals are of little evidential value. The fact is that in its effect

Studies in Asphyxia: I. Neuropathology Resulting from Comparatively Rapid Carbon-Monoxide Asphyxia

Studies in Asphyxia: I. Neuropathology Resulting from Comparatively Rapid Carbon-Monoxide Asphyxia