Quinolines attenuate PAF-induced pulmonary pressor responses and edema formation
Identifieur interne : 002711 ( Main/Exploration ); précédent : 002710; suivant : 002712Quinolines attenuate PAF-induced pulmonary pressor responses and edema formation
Auteurs : S. Falk [Allemagne] ; R. Göggel ; U. Heydasch ; F. Brasch ; K.-M. Müller ; A. Wendel ; S. UhligSource :
- American journal of respiratory and critical care medicine [ 1073-449X ] ; 1999.
Descripteurs français
- KwdFr :
- Acide acétylsalicylique (pharmacologie), Acides gras insaturés, Animaux, Benzoquinones (pharmacologie), Chloroquine (pharmacologie), Circulation pulmonaire (), Composés hétérocycliques bicycliques, Facteur d'activation plaquettaire (physiologie), Facteur de nécrose tumorale alpha (métabolisme), Femelle, Hydrazines (pharmacologie), Inhibiteurs de la lipoxygénase (pharmacologie), Inhibiteurs des cyclooxygénases (pharmacologie), Interleukine-6 (métabolisme), Mâle, Oedème pulmonaire (), Oedème pulmonaire (métabolisme), Oedème pulmonaire (physiopathologie), Perméabilité capillaire, Poumon (), Poumon (métabolisme), Quinidine (pharmacologie), Quinine (pharmacologie), Quinoléines (pharmacologie), Rat Wistar, Rats, Récepteur thromboxane (antagonistes et inhibiteurs), Résistance des voies aériennes, Résistance vasculaire, Souris, Souris de lignée BALB C, Techniques in vitro, Vasoconstriction ().
- MESH :
- antagonistes et inhibiteurs : Récepteur thromboxane.
- métabolisme : Facteur de nécrose tumorale alpha, Interleukine-6, Oedème pulmonaire, Poumon.
- pharmacologie : Acide acétylsalicylique, Benzoquinones, Chloroquine, Hydrazines, Inhibiteurs de la lipoxygénase, Inhibiteurs des cyclooxygénases, Quinidine, Quinine, Quinoléines.
- physiologie : Facteur d'activation plaquettaire.
- physiopathologie : Oedème pulmonaire.
- Pascal (Inist)
- Acides gras insaturés, Animaux, Circulation pulmonaire, Composés hétérocycliques bicycliques, Femelle, Mâle, Oedème, Oedème pulmonaire, Perméabilité capillaire, Poumon, Facteur activant thrombocyte, Facteur nécrose tumorale, Rat Wistar, Rats, Résistance des voies aériennes, Résistance vasculaire, Souris, Souris de lignée BALB C, Techniques in vitro, Vasoconstriction, Bronchoconstriction, Quinolone dérivé, Antibiotique, Physiopathologie, Exploration, Activité biologique, Animal, Rat.
- Wicri :
- topic : Antibiotique.
English descriptors
- KwdEn :
- Airway Resistance, Animal, Animals, Antibiotic, Aspirin (pharmacology), Benzoquinones (pharmacology), Biological activity, Bridged Bicyclo Compounds, Heterocyclic, Bronchoconstriction, Capillary Permeability, Chloroquine (pharmacology), Cyclooxygenase Inhibitors (pharmacology), Edema, Exploration, Fatty Acids, Unsaturated, Female, Hydrazines (pharmacology), In Vitro Techniques, Interleukin-6 (metabolism), Lipoxygenase Inhibitors (pharmacology), Lung, Lung (blood supply), Lung (metabolism), Male, Mice, Mice, Inbred BALB C, Pathophysiology, Platelet Activating Factor (physiology), Platelet activating factor, Pulmonary Circulation (drug effects), Pulmonary Edema (chemically induced), Pulmonary Edema (metabolism), Pulmonary Edema (physiopathology), Quinidine (pharmacology), Quinine (pharmacology), Quinolines (pharmacology), Quinolone derivatives, Rat, Rats, Rats, Wistar, Receptors, Thromboxane (antagonists & inhibitors), Tumor Necrosis Factor-alpha (metabolism), Tumor necrosis factor, Vascular Resistance, Vasoconstriction, Vasoconstriction (drug effects).
- MESH :
- chemical , antagonists & inhibitors : Receptors, Thromboxane.
- chemical , metabolism : Interleukin-6, Tumor Necrosis Factor-alpha.
- chemical , pharmacology : Aspirin, Benzoquinones, Chloroquine, Cyclooxygenase Inhibitors, Hydrazines, Lipoxygenase Inhibitors, Quinidine, Quinine, Quinolines.
- blood supply : Lung.
- chemically induced : Pulmonary Edema.
- drug effects : Pulmonary Circulation, Vasoconstriction.
- metabolism : Lung, Pulmonary Edema.
- chemical , physiology : Platelet Activating Factor.
- physiopathology : Pulmonary Edema.
- Airway Resistance, Animals, Bridged Bicyclo Compounds, Heterocyclic, Capillary Permeability, Fatty Acids, Unsaturated, Female, In Vitro Techniques, Male, Mice, Mice, Inbred BALB C, Rats, Rats, Wistar, Vascular Resistance.
Abstract
In the present study we have investigated the mechanisms of pulmonary edema caused by platelet-activating factor (PAF) in isolated rat lungs as well as in mice in vivo. In blood-free perfused and ventilated rat lungs, PAF increased lung weight by 0.59 ± 0.18 g. The cyclooxygenase inhibitor aspirin (500 μM) blocked this response by one-third, and the quinolines quinine (330 μM), quinidine (100 μM), and chloroquine (100 μM) by two-thirds. Lipoxygenase inhibition (10 μM AA861) alone or in combination with thromboxane receptor antagonism (10 μM SQ29548) had no effect on PAF-induced weight gain. In combination with aspirin, quinine or quinidine completely prevented PAF-induced weight gain and the concomitant increase of the capillary filtration coefficient (Kf,c). Pretreatment with quinine in vivo prevented not only PAF-, but also endotoxin-induced edema formation as assessed by Evans Blue extravasation. In addition, in vivo quinine prevented the endotoxin-induced release of tumor neurosis factor (TNF). Furthermore, in perfused lungs quinine reduced the PAF-induced increases in airway and vascular resistance, as well as thromboxane release. These findings demonstrate the following anti-inflammatory properties of quinolines: reduction of thromboxane and TNF formation; reduction of PAF-induced vasoconstriction and bronchoconstriction; and attenuation of PAF- and lipopolysaccharide (LPS)-induced edema formation. We conclude that the PAF-induced edema consists of two separate mechanisms, one dependent on an unknown cyclooxygenase metabolite, the other one sensitive to quinolines.
Affiliations:
- Allemagne
- Bade-Wurtemberg, District de Fribourg-en-Brisgau
- Constance (Allemagne)
- Université de Constance
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Le document en format XML
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Uhlig</name></author></analytic><series><title level="j" type="main">American journal of respiratory and critical care medicine</title><title level="j" type="abbreviated">Am. j. respir. crit. care med.</title><idno type="ISSN">1073-449X</idno><imprint><date when="1999">1999</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">American journal of respiratory and critical care medicine</title><title level="j" type="abbreviated">Am. j. respir. crit. care med.</title><idno type="ISSN">1073-449X</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Airway Resistance</term><term>Animal</term><term>Animals</term><term>Antibiotic</term><term>Aspirin (pharmacology)</term><term>Benzoquinones (pharmacology)</term><term>Biological activity</term><term>Bridged Bicyclo Compounds, Heterocyclic</term><term>Bronchoconstriction</term><term>Capillary Permeability</term><term>Chloroquine (pharmacology)</term><term>Cyclooxygenase Inhibitors (pharmacology)</term><term>Edema</term><term>Exploration</term><term>Fatty Acids, Unsaturated</term><term>Female</term><term>Hydrazines (pharmacology)</term><term>In Vitro Techniques</term><term>Interleukin-6 (metabolism)</term><term>Lipoxygenase Inhibitors (pharmacology)</term><term>Lung</term><term>Lung (blood supply)</term><term>Lung (metabolism)</term><term>Male</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>Pathophysiology</term><term>Platelet Activating Factor (physiology)</term><term>Platelet activating factor</term><term>Pulmonary Circulation (drug effects)</term><term>Pulmonary Edema (chemically induced)</term><term>Pulmonary Edema (metabolism)</term><term>Pulmonary Edema (physiopathology)</term><term>Quinidine (pharmacology)</term><term>Quinine (pharmacology)</term><term>Quinolines (pharmacology)</term><term>Quinolone derivatives</term><term>Rat</term><term>Rats</term><term>Rats, Wistar</term><term>Receptors, Thromboxane (antagonists & inhibitors)</term><term>Tumor Necrosis Factor-alpha (metabolism)</term><term>Tumor necrosis factor</term><term>Vascular Resistance</term><term>Vasoconstriction</term><term>Vasoconstriction (drug effects)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Acide acétylsalicylique (pharmacologie)</term><term>Acides gras insaturés</term><term>Animaux</term><term>Benzoquinones (pharmacologie)</term><term>Chloroquine (pharmacologie)</term><term>Circulation pulmonaire ()</term><term>Composés hétérocycliques bicycliques</term><term>Facteur d'activation plaquettaire (physiologie)</term><term>Facteur de nécrose tumorale alpha (métabolisme)</term><term>Femelle</term><term>Hydrazines (pharmacologie)</term><term>Inhibiteurs de la lipoxygénase (pharmacologie)</term><term>Inhibiteurs des cyclooxygénases (pharmacologie)</term><term>Interleukine-6 (métabolisme)</term><term>Mâle</term><term>Oedème pulmonaire ()</term><term>Oedème pulmonaire (métabolisme)</term><term>Oedème pulmonaire (physiopathologie)</term><term>Perméabilité capillaire</term><term>Poumon ()</term><term>Poumon (métabolisme)</term><term>Quinidine (pharmacologie)</term><term>Quinine (pharmacologie)</term><term>Quinoléines (pharmacologie)</term><term>Rat Wistar</term><term>Rats</term><term>Récepteur thromboxane (antagonistes et inhibiteurs)</term><term>Résistance des voies aériennes</term><term>Résistance vasculaire</term><term>Souris</term><term>Souris de lignée BALB C</term><term>Techniques in vitro</term><term>Vasoconstriction ()</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Receptors, Thromboxane</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Interleukin-6</term><term>Tumor Necrosis Factor-alpha</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Aspirin</term><term>Benzoquinones</term><term>Chloroquine</term><term>Cyclooxygenase Inhibitors</term><term>Hydrazines</term><term>Lipoxygenase Inhibitors</term><term>Quinidine</term><term>Quinine</term><term>Quinolines</term></keywords><keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Récepteur thromboxane</term></keywords><keywords scheme="MESH" qualifier="blood supply" xml:lang="en"><term>Lung</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Pulmonary Edema</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Pulmonary Circulation</term><term>Vasoconstriction</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Lung</term><term>Pulmonary Edema</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Facteur de nécrose tumorale alpha</term><term>Interleukine-6</term><term>Oedème pulmonaire</term><term>Poumon</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Acide acétylsalicylique</term><term>Benzoquinones</term><term>Chloroquine</term><term>Hydrazines</term><term>Inhibiteurs de la lipoxygénase</term><term>Inhibiteurs des cyclooxygénases</term><term>Quinidine</term><term>Quinine</term><term>Quinoléines</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Facteur d'activation plaquettaire</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Platelet Activating Factor</term></keywords><keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr"><term>Oedème pulmonaire</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Pulmonary Edema</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Airway Resistance</term><term>Animals</term><term>Bridged Bicyclo Compounds, Heterocyclic</term><term>Capillary Permeability</term><term>Fatty Acids, Unsaturated</term><term>Female</term><term>In Vitro Techniques</term><term>Male</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>Rats</term><term>Rats, Wistar</term><term>Vascular Resistance</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Acides gras insaturés</term><term>Animaux</term><term>Circulation pulmonaire</term><term>Composés hétérocycliques bicycliques</term><term>Femelle</term><term>Mâle</term><term>Oedème</term><term>Oedème pulmonaire</term><term>Perméabilité capillaire</term><term>Poumon</term><term>Facteur activant thrombocyte</term><term>Facteur nécrose tumorale</term><term>Rat Wistar</term><term>Rats</term><term>Résistance des voies aériennes</term><term>Résistance vasculaire</term><term>Souris</term><term>Souris de lignée BALB C</term><term>Techniques in vitro</term><term>Vasoconstriction</term><term>Bronchoconstriction</term><term>Quinolone dérivé</term><term>Antibiotique</term><term>Physiopathologie</term><term>Exploration</term><term>Activité biologique</term><term>Animal</term><term>Rat</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Antibiotique</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In the present study we have investigated the mechanisms of pulmonary edema caused by platelet-activating factor (PAF) in isolated rat lungs as well as in mice in vivo. In blood-free perfused and ventilated rat lungs, PAF increased lung weight by 0.59 ± 0.18 g. The cyclooxygenase inhibitor aspirin (500 μM) blocked this response by one-third, and the quinolines quinine (330 μM), quinidine (100 μM), and chloroquine (100 μM) by two-thirds. Lipoxygenase inhibition (10 μM AA861) alone or in combination with thromboxane receptor antagonism (10 μM SQ29548) had no effect on PAF-induced weight gain. In combination with aspirin, quinine or quinidine completely prevented PAF-induced weight gain and the concomitant increase of the capillary filtration coefficient (K<sub>f,c</sub>). Pretreatment with quinine in vivo prevented not only PAF-, but also endotoxin-induced edema formation as assessed by Evans Blue extravasation. In addition, in vivo quinine prevented the endotoxin-induced release of tumor neurosis factor (TNF). Furthermore, in perfused lungs quinine reduced the PAF-induced increases in airway and vascular resistance, as well as thromboxane release. These findings demonstrate the following anti-inflammatory properties of quinolines: reduction of thromboxane and TNF formation; reduction of PAF-induced vasoconstriction and bronchoconstriction; and attenuation of PAF- and lipopolysaccharide (LPS)-induced edema formation. We conclude that the PAF-induced edema consists of two separate mechanisms, one dependent on an unknown cyclooxygenase metabolite, the other one sensitive to quinolines.</div></front></TEI><affiliations><list><country><li>Allemagne</li></country><region><li>Bade-Wurtemberg</li><li>District de Fribourg-en-Brisgau</li></region><settlement><li>Constance (Allemagne)</li></settlement><orgName><li>Université de Constance</li></orgName></list><tree><noCountry><name sortKey="Brasch, F" sort="Brasch, F" uniqKey="Brasch F" first="F." last="Brasch">F. Brasch</name><name sortKey="Goggel, R" sort="Goggel, R" uniqKey="Goggel R" first="R." last="Göggel">R. Göggel</name><name sortKey="Heydasch, U" sort="Heydasch, U" uniqKey="Heydasch U" first="U." last="Heydasch">U. Heydasch</name><name sortKey="Muller, K M" sort="Muller, K M" uniqKey="Muller K" first="K.-M." last="Müller">K.-M. Müller</name><name sortKey="Uhlig, S" sort="Uhlig, S" uniqKey="Uhlig S" first="S." last="Uhlig">S. Uhlig</name><name sortKey="Wendel, A" sort="Wendel, A" uniqKey="Wendel A" first="A." last="Wendel">A. Wendel</name></noCountry><country name="Allemagne"><region name="Bade-Wurtemberg"><name sortKey="Falk, S" sort="Falk, S" uniqKey="Falk S" first="S." last="Falk">S. Falk</name></region><name sortKey="Falk, S" sort="Falk, S" uniqKey="Falk S" first="S." last="Falk">S. Falk</name><name sortKey="Falk, S" sort="Falk, S" uniqKey="Falk S" first="S." last="Falk">S. Falk</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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