Ammonia Inhalation Research Articles

Effects of ammonia inhalation on young cattle

Abstract Extract The trend toward confinement housing for dairy cattle has increased the problems associated with a variety of atmospheric contaminants. These noxious products include ammonia, hydrogen sulphide, carbon dioxide, sulphur dioxide, and methane as well as dust, organic acids and water vapour. The atmospheric concentration of ammonia is dependent upon many factors such as rate of animal excretion, water vapour level, temperature, ventilation and general management.

Radionuclidic Lung-Imaging Procedures in the Assessment of Injury due to Ammonia Inhalation

Clinical, physiologic, and bronchoscopic findings in a young man with acute injury of the respiratory tract due to inhalation of ammonia are described. Six months later, the patient's pulmonary function was reassessed by three radionuclidic lung-imaging procedures, which first revealed the sites and extent of the persisting obstructive disease processes. The diagnostic accuracy of the initial findings with radioactive xenon and aerosol were verified by the results of repeated bronchoscopic examination, bronchographic studies, standard pulmonary function tests, and lung-imaging procedures.

Role of trigeminal, olfactory, carotid sinus and aortic nerves in the respiratory and circulatory response to nasal inhalation of cigarette smoke and other irritants in the rabbit.

SummaryThe contributions of different afferent pathways to the reflex apnoea in expiration, mild hypertension and marked bradycardia evoked in unanaesthetized rabbits by nasal inhalation of cigarette smoke, formaldehyde, ammonia and benzene vapour were defined according to a factorial experimental design. Animals were used with (1) trigeminal nerve ablation, (2) olfactory bulb ablation, (3) total and selective section of the carotid sinus and aortic nerves, and (4) combinations of the above lesions. Trigeminal afferents are the primary source of the respiratory and circulatory disturbance. Olfactory afferents cannot initiate the respiratory and circulatory disturbance but weakly potentiate the apnoea induced by trigeminal stimulation. Arterial baroreceptor mechanisms contribute to the evoked bradycardia. Arterial chemoreceptor mechanisms do not contribute to the circulatory effects, but act to terminate the induced apnoea.

Retention of inhaled acetone and ammonia in the dog.

Acetone and ammonia are among the many compounds of toxicological interest found in the vapor phase of cigarette smoke. This study involves the handling of these compounds by the respiratory tract of the dog. Specific objectives included determination of uptake of each compound by the entire respiratory tract and by upper and lower portions under varying conditions of ventilatory rate, tidal volume, ad concentration inhaled. Uptake of acetone by the total respiratory tract ranged between 65 and 70% retention of ammonia was about 10% higher. In terms of regional uptake, retention of ammonia was higher than that of acetone in both the upper ad lower tracts. Experiments were also carried out to determine the effect of simultaneous inhalation of either acetone or ammonia with acetaldehyde on the respiratory uptake of acetaldehyde.

Effects of ammonia inhalation on respiration rate of rabbits.

Effects of ammonia inhalation on respiration rate of rabbits.

Hemodynamic effects of inhalation of ammonia in man

Inhalation of spirits of ammonia causes a reflex constriction of resistance blood vessels in the limbs, an increase in systemic arterial blood pressure and a reflex constriction of the capacitance vessels—all of which serve to raise cardiac filling pressure. These hemodynamic effects provide ample reason for the effectiveness of this traditional treatment for the common faint.

Respiratory ammonia filtration, mucous composition and ammonia tolerance in bats.

AbstractMaximum efficiency of removal of inhaled ammonia by respiratory mucous in three species of mammals has been determined by noting the increase above normal in plasma ammonia and urea nitrogen after exposing the blood in vivo and in vitro hightly ammoniated air. Guano bats, Tadarida brasiliensis, filtered 97.1% of the ammonia present in an inhaled mixture of 1130 PPM (parts per million ammonia). These bats further filtered 73.4% of a 4420 PPM in air mixture, 72.6% at 5040 PPM and 53.9% and 7200 PPM. For little brown bats, Myotis lucifugus, filtering efficiencies of 84.5% at 1330 PPM and 77.5% at 3010 PPM were found. Mice, Mus musculus, were found to filter 76.9% at 870 PPM. Efficiency of respiratory ammonia filtration relates directly to tolerance to inhaled ammonia in these mammals.Sodium, potassium, chloride, carbon dioxide, ammonia and urea nitrogen and protein levels in perfused respiratory tract fluid of the same three species after inhalation of ammonia in air mixtures are reported. In each species, ammonia and urea nitrogen levels in perfused respiratory tract fluid increases as inhaled concentrations of ammonia increase. In guano bats and little brown bats, carbon dioxide levels paralleled increases in ammonia apparently in sufficient quantity to provide the increase in buffering capacity necessary to neutralize absorbed ammonia. In mice, however, carbon dioxide levels dropped as inhaled ammonia levels increased. In no case did electrolyte or protein content change in any way to increase buffering capacity of respiratory mucous except in guano bats where protein levels rise consistently with inhaled ammonia concentrations.

Hemodynamic responses to ammonia inhalation in man: A powerful venoconstrictor stimulus

Hemodynamic responses to ammonia inhalation in man: A powerful venoconstrictor stimulus

HYPNOTICALLY-INDUCED "ANOSMIA" TO AMMONIA.

Abstract The procedure to demonstrate anosmia by the inhalation of ammonia is discussed. Deeply hypnotized Ss who are not knowledgeable of the relevant facts of physiology may fail to respond to ammonia fumes when it is suggested that they have no sense of smell (anosmia). However, persons who, in fact, are anosmic do respond to ammonia fumes because they are a powerful stimulus to the pain fibers in the nasal mucosa. This procedure illustrates that the crucial factor in the response of the hypnotized S is not the actual facts of anatomy and physiology, but the S's concept of them.

Ammonia Tolerance of the California Leaf-Nosed Bat

A series of 59 California leaf-nosed bats, Macrotus californicus, was exposed to varying concentrations of anhydrous ammonia. Physiologic responses noted in the bat were compared to the same responses as recorded in the literature for man and other experimental animals. Recordings were made for the following: cardiac and respiratory rates, blood non-protein nitrogen, urine urea and ammonia and animal and gassing chamber temperatures. An elevation of non-protein nitrogen over the mean normal was evident but no significant elevation of urine urea and ammonia was noted. Resistance to the gas was demonstrated by decreases in respiratory and cardiac rates. Toxic manifesta- tions attributable to ammonia were noted in distinct visceral damage, corrosion of the skin and mucous membranes and pulmonary edema. Maximum sublethal con- centration tolerated for an exposure time of 9 hours was 3,000 ppm. Investigators have often mentioned the extremely unpleasant working condi- tions in the ammoniated atmosphere of caves and mines frequented by large numbers of bats (Krutzch and Sulkin, 1958; Eads et al., 1955; many others). During certain times of the year concentrations of ammonia in Cueva del Tigre, 14.9 miles SSE, Carbo, Sonora, Mexico, are elevated to a level such that reflex res- piratory arrest was experienced by E. L. Cockrum (personal communication). The cave at this time was in use as a maternity colony for an estimated 2 to 3 million bats. Since this condition occurs in the normal habitat of these animals, interest was aroused regarding their unusual tolerance to ammonia. No in- formation has been presented on the physiologic response of a bat to ammonia concentrations. This study was made, therefore, to determine the physiologic effects of ammonia inhalation on the California leaf-nosed bat, Macrotus cali- fornicus Baird.

Respiratory reflex by intratracheal inhalation of ammonia gas and the brain stem reticular system.

Summary 1) In normal, decorticate, and decerebrate (with anterior and classical midcollicular sections) rabbits, an intratracheal inhalation of ammonia produced various respiratory patterns with increased or decreased rhythms and amplitudes leading to the inspiratory or expiratory breath-holding (see Table 1). After section of the vagal nerves these respiratory changes did not appear. 2) The changes of respiratory patterns evoked by ammonia inhalation were the same as those caused by electric stimulation of the brain stem reticular system. So the vagal nerves are considered to affect the respiratory renters in medulla oblongata, activating the brain stem reticular system. 3) In electronarcotized animals, this respiratory reflex shows almost the same changes as non-treated animals, but turns in reactions more or less dull and depressive. 4) Even in the cases of apneustic breathing inspiratory burst discharges are inhibited in rhythm and amplitude following ammonia inhalation.

Initial respiratory responses to the intratracheal inhalation of phosgene or ammonia.

1. The reflex responses to inhaled phosgene or ammonia vapour have been observed in tracheotomised dogs, cats and rabbits, and the most important findings are:(a) Ammonia and phosgene in high concentrations produce similar initial reactions, which are characteristic of each species and are mainly mediated by the vagi.(b) The dog appears to possess an extra‐vagal afferent system sensitive to such irritants, this system either being absent or much less sensitive in the cat and rabbit.(c) Bronchoconstriction is apparently induced by both gases in the absence of the central connexions of the vagus.2. From studies on the isolated blood‐perfused lungs of dogs, it is found that(a) Bronchoconstriction is produced by inhalation of either phosgene or ammonia.(b) The bronchoconstrictor action of ammonia is specifically potentiated by eserine, an effect which can be reversed by atropine.(c) The stimulating action of greater‐than‐threshold doses of ammonia in non‐eserinized lungs is not affected by atropine, nicotine or anthisan.3. From the evidence obtained in the second group of experiments, it is suggested that ammonia may have a direct stimulating action on the bronchial smooth muscle in addition to any action mediated by peripheral nervous structures and the release of acetylcholine.

Blood Changes Due to Ammonia Inhalation?

Blood Changes Due to Ammonia Inhalation?

The action of ammonia upon the lungs.

A study was made of rabbit and guinea pig lungs, and the effect of prolonged inhalation of ammonia in low concentration. The author used for this purpose a special apparatus, giving in the chamber a constant percentage of ammonia. Concentrations of 1.5, 0.5, 0.25 and 0.15 cc. of gaseous ammonia per liter of the chamber air were used. The experimental animals were kept in this chamber constantly until either death occurred or they were killed for examination. Their temperatures were taken daily, and they were weighed from time to time. Out of a total of 22 experimental animals, 3 rabbits and 11 guinea pigs died spontaneously, and 3 rabbits and 5 guinea pigs were killed. There was a rise of temperature in all the experimental animals exposed to concentrations of ammonia above 0.15 percent, which was usually more noticeable about the middle or toward the end of the period of exposure. The maximum rise was usually 0.3° to 2.5° C. above normal. The clinical symptoms produced were those of a pneumonia. Autopsy ...

On the presence of dextrose in the exudate of pulmonary edema

Injection of adrenalin causes glycosuria and hyperglycemia. In some instances the animals which receive adrenalin die of pulmonary edema. The chemical composition of the exudate of pulmonary edema has never been investigated. An examination of the exudate of rabbits which died from pulmonary edema after receiving adrenalin revealed the presence of a considerable amount of dextrose. The causation of pulmonary edema by the injection of adrenalin is, however, a matter of mere accident and cannot be relied upon in a systematic study. After various attempts we found that inhalation of ammonia can be fairly well relied upon to produce edema and produce it in a quantity sufficient to make a quantitative test for a reducing substance. The exudate did not clot, which shows that no pure blood was mixed with it. The number of experiments, although not yet large, permits a definite preliminary report. Besides analyzing the pulmonary exudate, in most cases a quantitative analysis of the blood for reducing substances was made and in some instances also of the urine. Pulmonary edema was also produced in two normal animals and in one animal which received an intravenous infusion of dextrose. The results may be briefly summarized as follows: The exudate of pulmonary edema contains dextrose or a reducing substance. The concentration seems to be in general equal to that of the blood. Two hours or longer after an intramuscular injection of adrenalin the exudate of the pulmonary edema may contain 0.5 per cent. and more of dextrose, a quantity, which, at least so far, usually slightly exceeded that of the corresponding blood.