Effects of sulfur dioxide on pore populations of canine tracheal epithelium

Man, S. F. Paul; Hulbert, William C.; Mok, Kelly; Ryan, Terence J.; Thomson, Abr

doi:10.1152/jappl.1986.60.2.416

Cited by 20 publications

(11 citation statements)

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“…A similar effect has been reported in dogs following exposure to SO 2 (Man et al, 1986). Frog palates which were incubated in ophiopogon root extract overnight prior to the application of sodium metabisulphite showed minimal to no discernable exfoliation and a corresponding beneficial effect on the recovery of mucociliary transport.…”

Section: Discussionsupporting

confidence: 77%

“…We have extended the previous applications of this model to create an epithelial injury model by applying a small volume of sodium metabisulphite on the palate. Sodium metabisulphite was chosen because it has been previously employed in other airway injury models (King, 1998;Man et al, 1986;Pon et al, 1994;Sakamoto et al, 1992). It has been shown to release SO 2 on contact with water and is therefore particularly suited for this application in addition to being a significant environmental pollutant.…”

Section: Introductionmentioning

confidence: 99%

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Ophiopogon root (Radix Ophiopogonis) prevents ultra-structural damage by SO2 in an epithelial injury model for studies of mucociliary transport

et al. 2004

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Section: Discussionsupporting

confidence: 77%

Section: Introductionmentioning

confidence: 99%

Ophiopogon root (Radix Ophiopogonis) prevents ultra-structural damage by SO2 in an epithelial injury model for studies of mucociliary transport

et al. 2004

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“…Enhanced permeability of the airway epithelium is related to the airway hyperresponsiveness to stimulants such as histamine. It has been reported that exposure to NO 2 (Ranga et al, 1980;Case et al, 1982;Gordon et al, 1980;Man etai, 1990), SO 2 (Norris and Jackson, 1989;Man et al, 1986;Vai et al, 1980), formaldehyde (Crocker and Bhalla, 1986), and acid (Holma, 1989) enhanced the permeability of tracheal or pulmonary epithelium. There is, however, only limited information about the effects of gaseous components and particulates in DE on the permeability of the nasal mucosal epithelium.…”

Section: Discussionmentioning

confidence: 99%

Short-Term Exposure to Diesel Exhaust Induces Nasal Mucosal Hyperresponsiveness to Histamine in Guinea Pigs

Kobayashi

Ikeue²,

Ito

et al. 1997

Toxicol Sci

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The increasing prevalence of allergic rhinitis in many countries is becoming a social problem. It is important to determine whether air pollutants are related to the increase in the prevalence rate of allergic rhinitis or not. In this respect, it is necessary to elucidate whether exposure to air pollutants affects the nasal mucosa and causes nasal mucosal hyperresponsiveness to chemical mediators released by antigen-antibody reactions. A previous study revealed that diesel exhaust particulates are potent in augmenting increases in nasal congestion and nasal secretion induced by histamine (T. Kobayashi and T. Ito, 1995, Fundam. Appl. Toxicol. 27,195-202). In the present study, using a rhinitis model of guinea pigs, we investigated whether short-term (3-hr) exposure to diesel exhaust induces nasal mucosal hyperresponsiveness to histamine. Guinea pigs of each group were exposed to filtered air or to a low or high concentration of diesel exhaust (1 and 3.2 mg/m 3 particulates in diluted diesel exhaust, respectively) for 3 hr. After diesel exhaust exposure, sneezing frequency, nasal secretion from the nostril, and intranasal airway resistance induced by histamine were measured as indices of sneezing response, rhinorrhea, and nasal congestion, respectively. Short-term exposure to a low or high concentration of diesel exhaust itself did not induce sneezing, nasal secretion, or nasal congestion. However, short-term exposure to a high concentration of diesel exhaust augmented sneezing and nasal secretion, but not nasal congestion, induced by histamine. In conclusion, short-term exposure to diesel exhaust potently induces nasal mucosal hyperresponsiveness. C 1997Socfc(jrofTajdco4ogy.The recent increase in the prevalence of allergic rhinitis (Kaneko et al, 1980;Crawford and Cohen, 1985;Aberg, 1989;Barbee et al, 1991;Lundback et al, 1992) in many countries is becoming an increasingly important social prob-' To whom correspondence and reprint requests should be addressed. Fax: 81-298-50-2439. lem. A positive relationship between the prevalence rate of allergic rhinitis and concentrations of atmospheric pollutants (Kaneko et al, 1980;Ishizaki et al, 1987) has been suggested from epidemiological studies. Therefore, it is important to clarify whether diesel exhaust (DE) could be related to the increase in the prevalence rate of allergic rhinitis. From this point of view, it is necessary to elucidate whether exposure to DE enhances IgE production and whether exposure to diesel exhaust particulates (DEP) causes nasal mucosal hyperresponsiveness to chemical mediators released by antigen-antibody reactions. It has been reported that administration of DEP or exposure to DE enhances IgE antibody production in mice (Muranaka et al, 1986;Takafuji et al, 1987;Fujimaki et al, 1994) and in humans (Diaz-Sanchez etal, 1994; Takenaka etal, 1995). In nasal hyperresponsive animals, increases in nasal airway resistance, nasal secretion, and sneezing elicited by major mediators released during an allergic attack were induced by the lowering ...

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“…This is speculative, although MBS-induced bronchoconstriction in the guinea-pig is partly mediated via NK 1 and NK 2 receptors [11]. In addition to its effects on sensory nerves, SO 2 at high concentrations (500 ppm, 75 min) causes focal loss of ciliated cells, a decrease in PD, and an increase in permeability of solutes up to the size of inulin across dog tracheal epithelium [26]. Our results are consistent, therefore, with the known actions of SO 2 .…”

Section: Mechanismsmentioning

confidence: 99%

Sodium metabisulphite causes epithelial damage and increases sheep tracheal blood flow and permeability

Wells

Hanafi²,

Jg³

1996

Eur Respir J

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Inhaled sodium metabisulphite (MBS) causes bronchoconstriction, cough and microvascular leakage. We have studied its effects on tracheal blood flow, potential difference (PD) and the permeability from tracheal lumen to venous blood of a low molecular weight hydrophilic tracer, 99m technetium-labelled diethylenetriamine penta-acetic acid ( 99m Tc-DTPA) in anaesthetized sheep.Flow was measured in a tracheal artery and blood from a cannulated tracheal vein collected for 5 min periods. The tracheal lumen was filled with Krebs-Henseleit solution (KH) containing 99m Tc-DTPA for six to eight 15 min periods. During the third or fourth period, MBS (1, 20 or 100 mM) was washed into the tracheal lumen for 15 min.MBS increased tracheal blood flow (venous flow (Q'v), 5-10 min MBS exposure period: 1 mM -9±18% (n=3); 20 mM +16±5% (n=5; p<0.05); 100 mM + 43±13% (n=5; p<0.05). It decreased PD in a concentration-dependent way. Venous 99m Tc-DTPA concentration increased progressively to +266±176 and + 958±321% 25-30 min after exposure to 20 and 100 mM MBS, respectively (p<0.05 for both). These effects were not blocked by luminal frusemide (3-7 mM) or flurbiprofen (100-500 µM). Histological sections showed changes to the epithelial cells and large intercellular spaces.Thus, luminal sodium metabisulphite increases tracheal blood flow, reduces transmural potential difference and causes tracheal epithelial damage, leading to an increase in 99m Tc-labelled diethylenetriamine penta-acetic acid permeability. Eur Respir J., 1996, 9, 976- Sodium metabisulphite (MBS) is a widely-used food preservative which, when ingested, causes bronchoconstriction in some asthmatics [1]. On inhalation it causes bronchoconstriction in man -asthmatics, atopics [2], and normals [3] -and also in animals [4,5].The mechanism of MBS-induced bronchoconstriction is still uncertain. In solution it forms the bisulphite ion and SO 2 [6]. Some [7], but not all [4,8], studies in man have shown that the bronchoconstriction is blocked by muscarinic antagonists. Its effect is also inhibited by drugs that inhibit sensory nerves, e.g. nedocromil sodium [9,10] and cromoglycate [9], and in the guinea-pig its action is reduced by capsaicin pretreatment [4] and inhibited by neurokinin 1 and 2 (NK 1 and NK 2 ) receptor antagonists [11], suggesting the involvement of tachykinins released from sensory nerve endings.MBS-induced bronchoconstriction is also blocked by frusemide [12,13]. Frusemide is effective against a variety of other indirectly acting bronchoconstrictor stimuli, including distilled water aerosols [14], exercise [15] and allergen [16]. The mechanism appears to be unrelated to its diuretic action. The airway effects could be due to the release of the bronchodilator prostaglandin E 2 (PGE 2 ) [17]. However, more recent evidence has shown that flurbiprofen, a cyclo-oxygenase inhibitor, partly blocks the effects of MBS on bronchoconstriction and also enhances the effect of frusemide [18]. This implies that MBS may cause the release of bronchoconstrictor prosta...

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Effects of sulfur dioxide on pore populations of canine tracheal epithelium

Cited by 20 publications

References 0 publications

Ophiopogon root (Radix Ophiopogonis) prevents ultra-structural damage by SO2 in an epithelial injury model for studies of mucociliary transport

Ophiopogon root (Radix Ophiopogonis) prevents ultra-structural damage by SO2 in an epithelial injury model for studies of mucociliary transport

Short-Term Exposure to Diesel Exhaust Induces Nasal Mucosal Hyperresponsiveness to Histamine in Guinea Pigs

Sodium metabisulphite causes epithelial damage and increases sheep tracheal blood flow and permeability

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