Nicotine Poisoning Research Articles

A further case of paroxysmal auricular fibrillation in acute nicotine poisoning.

Acta Medica ScandinavicaVolume 145, Issue 1 p. 28-33 A Further Case of Paroxysmal Auricular Fibrillation in Acute Nicotine Poisoning. BERTIL VON AHN, BERTIL VON AHN Medical Clinic, the Royal University, Uppsala, Sweden. (Head: Professor E. Ask-Upmark, M.D.)Search for more papers by this author BERTIL VON AHN, BERTIL VON AHN Medical Clinic, the Royal University, Uppsala, Sweden. (Head: Professor E. Ask-Upmark, M.D.)Search for more papers by this author First published: January/December 1953 https://doi.org/10.1111/j.0954-6820.1953.tb06992.xCitations: 3AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume145, Issue1January/December 1953Pages 28-33 RelatedInformation

Experimental studies in cardiovascular pathology. VII. Chronic nicotine poisoning in rats and in dogs: Hueper, W. C.: Arch. Path. 35: 846, 1943

Experimental studies in cardiovascular pathology. VII. Chronic nicotine poisoning in rats and in dogs: Hueper, W. C.: Arch. Path. 35: 846, 1943

The Role of the Augmented Epinephrine Secretion in Dogs after the Administration of Nicotine in the Fluctuation of the Arterial Blood Pressure and the Blood Sugar Con=centration Simultaneously Occurring

What a part is played in the organism of dogs in the nicotine in-toxication by the hypersecretion of epinephrine from the suprarelials taking place in that condition was tested in the present researches. The pattern of the adrenaline hydrochloride solution for imitating the natural output of epinephrine in the nicotine poisoning in animals; which are otherwise in the normal state, was the average of the figures obtained from the dogs, the output rate of which was determined in the conditions as physiological as possible and poisoned by an intra venous application of nicotine in the dose of 1mg. per kilo. Now some normal dogs were poisoned with that amount of nicotine, intravenously given in a short interval as in the previous investigations, utlized as the control. The arterial blood pressure was recorded by a mercury manometer, and the blood sugar was also determined from time to time. The dogs were never fastened, never narcotized. The same manipulations were done in some dogs, with the demedullat-ed suprarenals, otherwise wholly healthy. In the dogs so operated on, adrenaline hydrochloride solution was intravenously infused in the principle above given. Finally such dogs were given nicotine and ad-renaline hydrochloride together. The deprivation of the suprarenal medulla evokes some definite modification in the blood pressure curve and blood sugar fluctuation causable by the nicotine. Namely, the magnitude of hypertension is redendered a little smaller and especially the former half of the des-cending limb decidedly steeper by the demedullation of the glands. The magnitude of hyperglycemia, that is the maximum content and the duration of the hyperglycemia are cut short evidently by the deme-dullation. And the infusion of adrenaline hydrochloride solution in the man-ner just the same as that rate of epinephrine output during the nicotine intoxication just compensates these shortenings brought about by the depriviation of the epinephrine secretion from the suprarenals. The rôle of the augmented secretion of epinephrine in the nicotine intoxica-tion in causing the hyertension and hyperglycemia as well is thus first made clear. Further it is beyond doubt-this is also of high interest in delving the rôle of the epinephrine liberation-that the part played by the epinephrine secretion in bringing about the alterations-is distinctly dissimilar according to each; that is, the epinephrine secretion plays a rather smaller share in -causing the hypertension than other factors while a rather greater, or like share is played by it in the case of the hyperglycemia.

Nicotine poisoning in a child: By R. W. Cragg and A. E. Osterberg, Proc. Staff Meetings Mayo Clinic15: No. 37, Sept. 11, 1940

Nicotine poisoning in a child: By R. W. Cragg and A. E. Osterberg, Proc. Staff Meetings Mayo Clinic15: No. 37, Sept. 11, 1940

NICOTINE POISONING IN A CHILD

Nicotine is one of the most lethal poisons known to man. Some conception of its extreme toxicity may be gained by comparing it with hydrocyanic acid, which is of approximately equal potency. Nicotine is present in appreciable quantities in tobacco (ranging from 0.6 to 8 per cent),¹the poorer grades containing relatively more than the better grades. Since tobacco is used so widely both for smoking and for chewing (including snuff), it is amazing that so few instances of fatal poisoning from nicotine have been recorded. As far as smoking is concerned, a possible explanation may be the destruction of the drug by combustion and also its expulsion with the smoke. Then too, marked tolerance acquired by the habitual use of tobacco is undoubtedly an important factor. Consequently, in a majority of instances nicotine poisoning among adults has been traced to the ingestion of some strong solution of the

THE CONTROL OF NORMAL AND "CONVULSIVE" BRAIN POTENTIALS

Brain potentials can be used within limits as an index of the action of cerebral neurones. The recorded waves are the envelope of the beats of many single neurones and their profile depends on the shape of the unit potential and the temporal relation of the many units. The isolated frog brain, with relatively few and similar neurones which can be subjected to a wide variety of experimental conditions, is especially favorable for studying the control of potentials. Mammalian brain in situ, so far as similar experiments have been made, shows like behavior. The olfactory bulb of the isolated brain gives an electrical beat, at six per second, larger and more regular than before removal from the frog. Under varied conditions, the frequency, still regular, may be shifted from one to 50 per second and the single wave from a sine to many highly skewed forms constantly repeated. Such patterns indicate strong unison of the many cells and so reproduce the potential profile of the unit. The unit beat is controlled by the metabolism of the cell, oxidative or glycolytic energy supplying the driving force. It is also controlled by a trip mechanism, presumably the cell membrane, which determines the frequency of oscillation at constant drive. Amplitude and frequency vary inversely as the trip mechanism is altered, together as metabolism is changed. Control of cell potentials mainly through metabolism is considered in the cases of: oxygen lack, narcosis, cyanide, glucose lack, insulin, B1 avitaminosis, iodoacetate, and nicotine poisoning. The action and interaction of these and subsequent agents is presented. Control mainly through the trip mechanism is considered for: altered osmotic pressure, sodium, potassium, calcium, magnesium, and hydrogen ions; for neural stimulation and, in more detail, for polarization by constant currents. Unification of the beats of the many units into synchronous or simultaneous patterns must depend on the propagation of nerve impulses or on electric fields and currents. The mechanism of unification is analyzed and tests for its effectiveness are described. The following conditions favor unison: high temperature and calcium, low potassium and sodium, diminution in afferent nerve impulses (in patterns), increased polarization (or injury potentials), the drugs nicotine and caffeine. Further analysis is made with caffeine, which leads to large repeated waves which may travel along the hemisphere. These are described in detail; and also the control of their size, shape, frequency, speed, and direction of travel by temperature and polarization. The spreading caffeine waves are not stopped by nicotine, which blocks synaptic conduction; they cross a complete transection of the hemisphere when the two halves are in good apposition and so in electrical but not neural continuity; and a caffeinized brain can augment the activity of an abutting normal one. It is concluded that, besides neural coordination of separate neurons, a strictly electrical mechanism can regulate nerve cell beats and cause a spreading activation. This may prove of considerable importance in the interpretation of normal activity, electronarcosis, and of the massed "convulsive" action of the cortex in epilepsy. A theoretical explanation of the mechanism of spread is presented. It demands the existence in brain of maintained polarization gradients in certain directions. These have been found present as predicted.

Japan Institute for Science of Labour

THE annual report of the director of the Japan Institute for Science of Labour for 1937 gives a brief account of the history of the Institute as well as of its divisions and functions (Tokyo: Japan Institute for Science of Labour, 1938. 70 sen). A programme of proposed investigations, including studies on nutrition and the prevention of industrial accidents and occupational disease, is also outlined which indicates how sadly warped the whole outlook of Japan has become under the demands of her policy of war and aggression. Brief notes are included on investigations completed in 1936–37, among which may be mentioned a study of dust in mail-cars and a survey of the labour conditions of railway postal workers. The first part of an investigation on gaseous metabolism in heavy muscular work has been completed, covering gaseous exchange in static effort, and a third report on occupational diseases of printers, especially lead poisoning, deals with the density of dust ïn the air and the window space in the printing shop. A statistical analysis has been made of the causes of death in different occupations, and other studies have included acute nicotine poisoning among land workers and water supply in an agricultural village.

Nicotine intoxication and pregnancy: Morra, Giuseppe: Ginecologia (Torino) 9: 996, 1935

Nicotine intoxication and pregnancy: Morra, Giuseppe: Ginecologia (Torino) 9: 996, 1935

A Further Study of the Augmenting Action of Nictine upon the Epinephrine Secretion from the Suprarenals of the Non=Anaesthetized Dog

Influence of nicotine upon the epinephrine output rate, the mean arterial blood pressure and the blood sugar concentration were determined in the dogs, non-fastened, non-anaesthetized, without evoking pain. Although the epinephrine output was measured by Watanabe in the dogs, in physiological conditions as normal as possible, other than nicotine poisoning, the short interval of time just after injection was regrettably omitted there, owing to difficulties of managing the animal in the intoxication period. But this time is in fact just that betraying a maximally accelerated secretion of epinephrine, judging from the experiments undertaken under narcosis. Our expectation has been realized, the blood samples from the suprarenals, collected 30 seconds long from the moment of starting injection (1 mgrm. nicotine per kilo intravenously), showed the maximum acceleration. The absolute value was 0.01 mgrm.-0.0007 mgrm. per kilo per minute from the one gland, or several hundreds to seventy times the preinjection rate. That in the second or subsequent 30 seconds period was about two-thirds of the preceding period, then afterwards it diminished quickly, so that usually about 5-10 minutes later the epinephrine output rate was found almost similar to the pre-injection period. But this length of the hyperepinephrinaemic period is thus far longer in nonanaesthetized dogs, compared to the animals under narcosis. The period of the great acceleration must be taken as very brusque. The period of the largest acceleration in the epinephrine liberation corresponds to the spell where the blood pressure fell abruptly, and at the end of this first 30 seconds period the pressure set in to elevate, and in the second 30 seconds period the elevation reached its maximum. Thus it may be comprehensible that the maximum acceleration in the epinephrine discharge occurs almost simultaneously with the blood pressure fall and precedes the pressure elevation. The changes in the blood sugar concentration occurred more slowly than those in the arterial pressure. The denervation of the suprarenal gland, -there the splanchnic nerves were cut-, caused some diminution in the acceleration of the epinephrine output rate if the figures obtained in one and the same dog, one gland with the intact innervation, another denervated, be compared with each other. This finding might be explained by assuming some action of nicotine on the nervous mechanism for regulating the epinephrine liberation, besides on the suprarenal medulla. But the authors will not pronounce it now because of the smallness of experience.

Acute nicotine poisoning: Report of a case in a child

<h2>Summary</h2> Although acute nicotine poisoning appears to be a relatively rare disease, the frequent exposure of children to tobacco in the American home makes it a clinical entity with which every physician should be familiar. The possibility of acute nicotine poisoning should be strongly considered in all cases of undiagnosed coma. An attempt to elicit a history of contact with nicotine should always be made in these cases, for there is a possibility that many of these cases have occurred with a failure of diagnosis. The classical experiments mentioned have established the definite therapeutic value of artificial respiration and the injection of epinephrine in cases where the heart has stopped beating. It might be suggested that the mechanical respirator would furnish the ideal method of carrying on respiration in these cases until the temporary paralysis of the involved respiratory muscles has subsided.

THE TREATMENT OF ACUTE NICOTINE POISONING

The fact that an individual poisoned with nicotine is rarely seen by the physician in time to institute treatment is not a sufficient reason for a lack of knowledge as to what may be done to save life when the opportunity is at hand. Except for the usual procedures to remove any unabsorbed poison and the administration of stimulants, we have been unable to find in the literature any description of a rational treatment for nicotine poisoning. Generally the condition is considered hopeless. This pessimistic attitude is apparently due to the belief that the drug causes generalized paralysis of the central nervous system, based on the fact that complete muscular paralysis, loss of reflexes and paralysis of respiration (and finally of circulation) follow its absorption in sufficiently large doses. As Moore and Rowe1have pointed out, all these effects could as readily be due to the curare-like action of the drug as to central paralysis. As a result of experiments on dogs,2we are convinced that death from nicotine poisoning is due to peripheral paralysis of the respiratory muscles when convulsions are prevented, and, if these occur, to fixation of the respiratory muscles.

NICOTINE POISONING BY ABSORPTION THROUGH THE SKIN

Nicotine is one of the most deadly poisons known to man and, at the same time, one with which he comes into most intimate contact in his daily life. It is somewhat surprising, therefore, that serious cases of nicotine poisoning are not reported more frequently. The main reasons for the infrequency of serious poisoning are that the percentage of nicotine in tobacco is too small to make it easy to get a fatal dose from the ingestion of tobacco or the inhalation of its smoke, and that nausea and vomiting are early symptoms which ordinarily prevent further absorption of the drug. Fatal poisoning from tobacco, although rare, has been reported from smoking, from swallowing tobacco, from tobacco enemas, and from its use as a local application to the skin in favus.1The commercial insecticides that contain high percentages of nicotine are, of course, far more dangerous. McNally2has

What harmful effects does nicotine cause in blood vessels? N. Kahler (Die Aerztliche Praxis, No. 1, 1929)

The author of the book answers this question, nicotine causes vasospasm in all organs and especially in the brain; This spasm may underlie the frequently observed migraines, fainting conditions, aphasia, and other diseases; nicotine poisoning often causes vasomotor angina pectoris, intermittent spasms of the vessels of the abdominal cavity, proceeding under the guise of ileus, spasms of the esophagus, pyloric part of the stomach, intestines; finally, nicotine plays an important role in the development of increased gastric acidity of impotence, intermittent claudication of the extremities, diseases of Brger'a and Raynaud.

Paroxysmal ventricular tachycardia: A report of five cases

Paroxysmal ventricular tachycardia is more common than the number of reported cases would indicate. Five cases are described, illustrating different causes for the attacks. In two, the subjects of advanced myocardial disease with steadily progressing congestive failure, digitalis was the provoking cause of the attacks. The dose of digitalis did not exceed that calculated by the body-weight method of Eggleston. It is concluded that this disorder of rhythm depends more upon the state of cardiac nutrition than upon the degree of concentration of the drug in the tissues. It is suggested that a mechanism, similar to that which underlies the production of auricular fibrillation by digitalis in cases of heart disease with normal rhythm, may also be present in these cases where the drug has provoked ventricular tachycardia. In one case, nicotine intoxication was regarded as an important factor in the production of this arhythmia. Advanced coronary sclerosis and myocardial disease were present in one case, and in the last case no demonstrable cause could be found. Quinidine sulphate was of value in controlling the paroxysms in this case. The prognosis is briefly discussed and emphasis is placed upon closely watching the heart rate in all cases of advanced myocardial failure under treatment with digitalis.

Nicotine poisoning of the inner ear; a preliminary report from animal experimentation and microscopic findings. (From the physiological department of columbia university.)

Nicotine poisoning of the inner ear; a preliminary report from animal experimentation and microscopic findings. (From the physiological department of columbia university.)

Cases of nicotine and belladonna poisoning in the dog

Cases of nicotine and belladonna poisoning in the dog