scholarly journals The Biological Mechanisms of Air Ion Action

1960 ◽  
Vol 43 (3) ◽  
pp. 533-540 ◽  
Author(s):  
Albert P. Krueger ◽  
Richard F. Smith

Intravenous administration of 5-hydroxytryptamine to rabbits and guinea pigs is shown to bring about changes very similar to those produced by (+) air ions, including (1) decreased ciliary rate, (2) contraction of the posterior tracheal wall, (3) exaggerated response of the tracheal mucosa to trauma, (4) marked vasoconstriction in the tracheal wall, and (5) increased respiratory rate. These effects are reversed by (-) air ions. Iproniazid, which raises 5-hydroxytryptamine levels in the animal by blocking monamine oxidase, produces similar but non-reversible effects. Reserpine, which depletes 5-hydroxytryptamine in the animal, causes changes that resemble those produced by (-) air ions, including (1) increased ciliary rate, (2) relaxed posterior sulcus, (3) hyperemia of the tracheal mucosa, (4) lowered respiratory rate, and (5) increased volume and rate of mucus flow. On the basis of these facts, the hypothesis is advanced that (+) air ion effects are mediated by the release of free 5-hydroxytryptamine, while (-) air ion effects depend on the ability of (-) ions to accelerate the enzymatic oxidation of 5-hydroxytryptamine.

1960 ◽  
Vol 44 (2) ◽  
pp. 269-276 ◽  
Author(s):  
Albert P. Krueger ◽  
Richard F. Smith ◽  

Negative air ions are shown to decrease 5-hydroxytryptamine concentrations in extirpated strips of rabbit trachea and in the respiratory tracts of living mice. An initial exposure of guinea pigs to (-) air ions causes a transient rise in urinary 5-hydroxyindoleacetic acid excretion which is not observed upon subsequent exposures. These findings are compatible with the hypothesis advanced earlier that (-) air ion effects depend on the ability of (-) ions to accelerate enzymatic oxidation of 5-hydroxytryptamine.


1959 ◽  
Vol 42 (5) ◽  
pp. 959-969 ◽  
Author(s):  
Albert P. Krueger ◽  
Richard F. Smith

A. Duration of Effects Groups of mice exposed to high densities of unipolar light air ions for 72 hours exhibited persistent alterations in the functional efficiency of their tracheas. These effects lasted at least 4 weeks, and in the case of animals treated with (+) ions included diminished ciliary activity, pale and contracted tracheal mucosa, and enhanced vulnerability to trauma. Following treatment with (-) ions, animals displayed increased ciliary activity with no other detectable changes. It required at least 60 minutes of exposure to ions to induce such "permanent" functional changes. B. Minimal Effective Ion Densities The minimal ion densities producing changes in ciliary activity within an arbitrary period of 30 minutes were determined with extirpated tracheal strips from rabbits and guinea pigs. The threshold value for (-) ions was approximately 2.5 x 103 ions/cm.2/sec. and that for (+) ions was in the range between 1 x 104 and 2.5 x 105 ions/cm.2. The minimal ion densities producing changes in ciliary activity within an arbitrary period of 30 minutes were determined with extirpated tracheal strips from rabbits and guinea pigs. The threshold value for (-) ions was approximately 2.5 x 103 ions/cm.2/sec. and that for (+) ions was in the range between 1 x 104 and 2.5 x 105 ions/cm.2. The evidence indicates that ion-induced functional changes in the ciliated epithelium of the pulmonary tree are the results of direct contact of ions with surface cells and do not involve participation of the central nervous system or circulation. So far as ciliary activity is concerned, the number of ions required to produce a change in rate is very small.


1958 ◽  
Vol 42 (1) ◽  
pp. 69-82 ◽  
Author(s):  
Albert P. Krueger ◽  
Richard F. Smith

Studies on the effects of air ions on the functional efficiency of the extirpated tracheal strip have been extended to the trachea of the living rabbit, rat, and mouse. Animals exposed to high mobility (+) air ions administered via a tracheotomy aperture displayed: (a) Decreased ciliary activity. (b) Decline in mucus flow rate, sometimes reversed by prolonged exposure to (+) ions; a frequent drop in the volume of mucous secretion. (c) Contraction of the membranous posterior tracheal wall. (d) Increased vulnerability to trauma of cilia and mucosal blood vessels. Similar treatment with (-) air ions reversed (+) ion effects on ciliary activity, mucus flow, contraction of the tracheal smooth muscle. Continued (-) ion treatment raised the ciliary rate (invariably) and the mucus flow rate (often) above their initial levels. (+) Air ions administered to unoperated resting mice and rats increased the respiratory rate; (-) ions reversed this effect. Long exposure of unoperated ambulatory mice to (+) air ions produced: (a) Decreased ciliary activity. (b) No clear cut effect on mucus flow. (c) Contraction of the posterior tracheal wall. (d) Increased vulnerability of the mucosa to trauma. (-) Air ions increased ciliary activity but had no clear-cut effect on the mucus flow rate.


1986 ◽  
Vol 56 (03) ◽  
pp. 311-317 ◽  
Author(s):  
P A Barrett ◽  
K D Butler ◽  
R A Shand ◽  
R B Wallis

SummaryIntravenous administration of arachidonic acid to guinea-pigs caused a dose-related, rapid accumulation of 51Cr-labelled platelets in the thorax. Inhibitors of cyclooxygenase inhibited the platelet accumulation, induced by arachidonic acid (30 mg/kg), at doses which did not alter the thoracic blood volume (as measured by 131I-labelled human albumin). Thromboxane synthetase inhibitors had different effects on platelet accumulation depending on the dose. CGS 12970 (3 mg/kg) and N(1-carboxyheptyl) imidazole (100 mg/kg) reduced platelet accumulation. High doses of CGS 12970 and CGS 13080 caused an apparent enhancement of platelet accumulation which was associated with pooling of blood in the thorax, as measured by either 131I-labelled human albumin or 51Cr-labelled erythrocytes. This increase in thoracic blood volume was abolished if the guinea-pigs were also pretreated with diclofenac (1 mg/kg) in addition to the thromboxane synthetase inhibitor. Increases in thoracic blood volume were also obtained following infusions of PGI2 but not PGD2 or PGE2.


ORL ◽  
2000 ◽  
Vol 62 (3) ◽  
pp. 167-169 ◽  
Author(s):  
Philipp Dost ◽  
Norbert Thürauf ◽  
Wolf Armbruster ◽  
Beate Schoch ◽  
Martin Zülke ◽  
...  

2018 ◽  
Vol 314 (3) ◽  
pp. R489-R498 ◽  
Author(s):  
Yang-Ling Chou ◽  
Nanako Mori ◽  
Brendan J. Canning

We have addressed the hypothesis that the opposing effects of bronchopulmonary C-fiber activation on cough are attributable to the activation of C-fiber subtypes. Coughing was evoked in anesthetized guinea pigs by citric acid (0.001–2 M) applied topically in 100-µl aliquots to the tracheal mucosa. In control preparations, citric acid evoked 10 ± 1 coughs cumulatively. Selective activation of the pulmonary C fibers arising from the nodose ganglia with either aerosols or continuous intravenous infusion of adenosine or the 5-HT3 receptor-selective agonist 2-methyl-5-HT nearly abolished coughing evoked subsequently by topical citric acid challenge. Delivering adenosine or 2-methyl-5-HT directly to the tracheal mucosa (where few if any nodose C fibers terminate) was without effect on citric acid-evoked cough. These actions of pulmonary administration of adenosine and 2-methyl-5-HT were accompanied by an increase in respiratory rate, but it is unlikely that the change in respiratory pattern caused the decrease in coughing, as the rapidly adapting receptor stimulant histamine also produced a marked tachypnea but was without effect on cough. In awake guinea pigs, adenosine failed to evoke coughing but reduced coughing induced by the nonselective C-fiber stimulant capsaicin. We conclude that bronchopulmonary C-fiber subtypes in guinea pigs have opposing effects on cough, with airway C fibers arising from the jugular ganglia initiating and/or sensitizing the cough reflex and the intrapulmonary C fibers arising from the nodose ganglia actively inhibiting cough upon activation.


1991 ◽  
Vol 62 (3) ◽  
pp. 126-129
Author(s):  
J. Hattingh ◽  
N. I. Pitts ◽  
V. De Vos ◽  
D. G. Moyes ◽  
M. F. Ganhao

The time which elapses before cessation of breathing, and blood pressure and blood gas changes after the intramuscular administration of suxamethonium, or a mixture of suxamethonium and hexamethonium, is compared in immobilised African elephants (Loxodonta africana) and buffaloes (Syncerus caffer). In addition, the respiratory responses of elephants and other animals to intravenous administration of suxamethonium and succinylmonocholine are reported on, as are the effects of darting animals with succinylmonocholine. The results show that respiration is affected in a similar fashion in all species investigated. However, the characteristic gradual decrease in respiratory rate seen in elephants during culling, using suxamethonium, resembles the effects observed when succinylmonocholine is administered. It is suggested that elephants are killed by this first breakdown product of suxamethonium during culling and/or that unique acetylcholine receptors may be involved.


2007 ◽  
Vol 86 (9) ◽  
pp. 546-548 ◽  
Author(s):  
Jason S. Hamilton ◽  
Sofia Avitia ◽  
Ryan F. Osborne

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