186,284 research outputs found
HYDROPEROXIDE-INDUCED BRONCHOCONSTRICTION AND VASOCONSTRICTION IN THE ISOLATED RAT LUNG
No full textThe effects of different hydroperoxides on lung mechanics and perfusate flow rate and their mechanisms of action were studied in isolated perfused rat lungs. The administration of hydrogen peroxide, t-butyl hydroperoxide, cumene hydroperoxide, linoleic acid hydroperoxide, and linoleic acid ethylester hydroperoxide (0.1-2 mM) to the perfusate caused a marked decreased in lung compliance, conductance, and perfusate flow rate, with constriction strength of t-butyl hydroperoxide > hydrogen peroxide > cumene hydro-peroxide > linoleic acid ethylester hydroperoxide > linoleic acid hydroperoxide. Although the hydroperoxides probably had to enter lung cells to exert their effects, no relationship was found between constriction strength and amount of hydroperoxide taken up by the lung. Reduced sensitivity was apparent after repeated dosing, depending on the length of time between dosing. The addition of the iron chelator Desferal (1 mM) had no effect on the hydroperoxide-induced broncho- and vasoconstriction, although free iron was reduced by 50% in the lungs. The administration of the antioxidants diphenyl-p-phenylenediamine (50-mu-M) or butylated hydroxyanisole (200-mu-M) to the perfusate 20 min prior to the hydroperoxide attenuated the hydroperoxide-induced effects as well as arachidonic acid-induced broncho- and vasoconstruction. Our findings have shown that hydroperoxides that can enter the lung cells will also induce both vaso- and bronchoconstriction in the isolated perfused rat lung
ALTERNATIVE PATHWAYS OF SULFITE OXIDATION IN HUMAN POLYMORPHONUCLEAR LEUKOCYTES
No full textSodium sulfite is metabolized by human polymorphonuclear leukocytes by two alternative pathways, one enzymatic route dependent on sulfite oxidase and one non-enzymatic which involves intermediate formation of sulfur trioxide anion radicals. Initiation of the oxidative burst by phorbol myristate acetate significantly stimulates sulfate formation through the second pathway. The activity of sulfite oxidase in polymorphonuclear leukocytes varies greatly among individuals, a variation consistent with the suggested polymorphic distribution of sulfite oxidase in the human population
SULFUR DIOXIDE-INDUCED BRONCHOCONSTRICTION IN THE ISOLATED PERFUSED AND VENTILATED GUINEA-PIG LUNG
No full textSO2 exposure (50-500 ppm) of isolated, perfused and ventilated guinea pig lungs, via the air passages, caused a concentration-related reduction in dynamic compliance and conductance. No changes in pulmonary perfusion flow was noted at any SO2 concentration. Formed sulfite was detected in lung lavage fluid as well as in the perfusate. Pretreatment of the lungs with a low concentration of SO2 (10 ppm) for 30 min protected against bronchoconstriction by a high concentration of SO2 (250 ppm). A similar protective effect was noted by pretreatment with sodium sulfite (3 mM) in the lung perfusate
VASOCONSTRICTION AND BRONCHOCONSTRICTION INDUCED BY 2,5-DI-(TERT-BUTYL)1,4-BENZOHYDROQUINONE, AN ENDOPLASMIC RETICULAR CA2+-ATPASE INHIBITOR, IN ISOLATED AND PERFUSED RAT LUNG
No full textThe microsomal Ca2+-ATPase inhibitor 2,5-di-(tert-butyl)-1,4-benzohydroquinone (tBuBHQ) induced bronchoconstriction and vasoconstriction in the isolated perfused and ventilated rat lung. Thes effects were accompanied by increased levels of thromboxane and prostacyclin in the effluent perfusate. The effect of tBuBHQ was inhibited by L-655,240, a thromboxane receptor antagonist, indicating thromboxane-A2-mediated bronchoconstriction and vasoconstriction. Accordingly, the cyclooxygenase inhibitor indomethacin largely blocked the effects of tBuBHQ. The involvement of a phospholipase in the generation of thromboxane A2 (TXA2) was supported by dibucaine protection on tBuBHQ effects. The results from this study indicate that tBuBHQ, probably by inhibiting the microsomal Ca2+-ATPase, can trigger the arachidonic acid cascade leading to the formation of TXA2, which in turn causes bronchoconstriction and vasoconstriction in rat lung
MODIFICATIONS OF CELLULAR THIOLS DURING GROWTH AND SQUAMOUS DIFFERENTIATION OF CULTURED HUMAN BRONCHIAL EPITHELIAL-CELLS
No full textThiol modifications during growth and differentiation of cultured normal human bronchial epithelial cells was studied by analysis of their content and redox state of low-molecular-weight thiols and protein thiols. Subculture of the cells with trypsin decreased the cellular content of the major low-molecular-weight thiol, i.e., reduced glutathione, although the glutathione content had returned to levels comparable to those before subculture already after 4 h in conjunction with cell attachment. During subsequent culture, increases in the cellular contents of glutathione, total cysteine equivalents, and total protein thiols occurred. These modifications in the amounts and redox balance of thiols were transient and preceded the major growth phase. Exposure of cells at clonal density to either diethylmaleate, a thiol-depleting agent, or buthionine sulfoximine, an inhibitor of glutathione synthesis, decreased the proliferative ability of the cells as demonstrated by a markedly decreased colony forming efficiency. Moreover, in mass cultures exposed to buthionine sulfoximine, a marked depletion of the glutathione content was again accompanied by inhibition of growth. Exposure of the cells to agents known to induce growth arrest and terminal squamous differentiation, i.e., fetal bovine serum, Ca2+, or transforming growth factor-beta 1, resulted in increased levels of reduced glutathione. No consistent alteration in the contents of the other thiols was noted. Overall, the results demonstrate consistent variations in the amounts and redox state of cellular thiols, particularly reduced glutathione, supporting a role of thiols in regulation of growth and squamous differentiation of human bronchial epithelial cells. (C) 1994 Academic Press, Inc
Author-wise bibliometric analysis based on entropy.
No full textAuthor-wise bibliometric analysis based on entropy.</p
SULFUR DIOXIDE-INDUCED BRONCHOCONSTRICTION VIA RUTHENIUM RED-SENSITIVE ACTIVATION OF SENSORY NERVES
No full textThe mechanism of sulfur dioxide-induced bronchoconstriction was studied using isolated perfused and ventilated guinea-pig lungs. They were exposed to sulfur dioxide after pretreatment with different compounds, either via the pulmonary artery or via the air passages. Neither the cyclooxygenase inhibitor indomethacin (30 muM) nor the H-1-receptor antagonist diphenhydramine (15 muM), given via the perfusate, attenuated the sulfur dioxide-induced bronchoconstriction. Furthermore, sulfur dioxide exposure did not cause a release of either thromboxane or histamine into the perfusate. In experiments with atropine equivocal results were obtained with regard to protection against sulfur dioxide-evoked bronchoconstriction. Intratracheal instillation of the local anesthetic agent lidocaine (1 mg/50 mul) markedly reduced the sulfur dioxide-induced bronchoconstriction. Also, ruthenium red (10 muM), an agent with calcium entry-blocking properties and an inhibitor of capsaicin-induced bronchoconstriction, was able to inhibit the effect of sulfur dioxide. The sulfur dioxide-induced bronchoconstriction was associated with release of calcitonine gene-related peptide, a sensory neuropeptide. The effect of sulfur dioxide was also inhibited by a Ca2+-free buffer plus EGTA. These results suggest that sulfur dioxide-induced bronchoconstriction in the guinea-pig lung is the result of a local effect on sensory nerves (C-fiber activation). The mechanism seems to be dependent on the Ca2+-dependent release of sensory neuropeptides and to be linked to opening of the cation channel, which is associated with the proposed capsaicin receptor on sensory nerves as revealed by the inhibitory effect of ruthenium red
Going Beyond Counting First Authors in Author Co-citation Analysis
No full textThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
SULFUR-DIOXIDE AND SODIUM METABISULFITE INDUCE BRONCHOCONSTRICTION IN THE ISOLATED-PERFUSED AND VENTILATED GUINEA-PIG LUNG VIA STIMULATION OF CAPSAICIN-SENSITIVE SENSORY NERVES
No full textIn this study the relationship between sulfur dioxide-induced sensory nerve activation and acute bronchoconstriction was assessed. We also studied the effects of sodium metabisulfite, an agent that is suggested to increase airway resistance via activation of sensory nerves. Sulfur dioxide (250 ppm) induced a characteristic biphasic bronchoconstriction. Concomitantly sulfur dioxide induced the release of calcitonin gene-related peptide (CGRP) from capsaicin-sensitive sensory nerves into the pulmonary circulation. In lungs of guinea pi,os pretreated with a neurotoxic dose of capsaicin, the first phase of bronchoconstriction was reduced and the overflow of CGRP was not detectable. Tetrodotoxin abolished the initial phase of the bronchoconstriction induced by sulfur dioxide, indicating that a local neural reflex depending on sodium channels was operant. Inhibition of the vanilloid receptor with capsazepine slightly, although not significantly, reduced the contractile responses to sulfur dioxide. Sodium metabisulfite, when infused via the pulmonary circulation (3 mM), induced bronchoconstriction which was abolished by capsaicin pretreatment, but not significantly reduced by capsazepine. The results indicate that in the isolated guinea pig lung inhaled sulfur dioxide induces initial bronchoconstriction in part via sensory nerve activation, while other mechanisms are involved in the late effect. Sensory nerve activation appears to be the only mechanism for bronchoconstriction induced by infused sodium metabisulfite. A role for sensory nerve-mediated bronchoconstriction by sulfur dioxide or sodium metabisulfite via activation of the vanilloid receptor could not be conclusively demonstrated by this study using capsazepine
Sodium Metabisulfite and citric acid induce bronchoconstriction via a sulfite sensitive pathway in the isolate guinea pig lung
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