Vascular protein leakage in various tissues induced by substance P, capsaicin, bradykinin, serotonin, histamine and by antigen challenge

Saria, Alois; Lundberg, Jan M.; Skofitsch, Gerhard; Lembeck, Fred

doi:10.1007/bf00503897

Cited by 410 publications

(158 citation statements)

References 28 publications

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“…Though not in every experimental condition (Ingenito et al, 1991), the involvement of capsaicin-sensitive fibres in models of allergy is well established (Saria et al, 1983;Manzini et al, 1987;Alving et al, 1987;Gentilini et al, 1990c;Kohrogi et al, 1991). This was also confirmed under our experimental conditions, where depletion of neuropeptide-containing terminals by superfusion with capsaicin reduced the tracheal strip response to OA.…”

Section: Discussionsupporting

confidence: 84%

GABA‐mediated inhibition of the anaphylactic response in the guinea‐pig trachea

Gentilini

Franchi‐Micheli

Mugnai

et al. 1995

British J Pharmacology

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In sensitized guinea‐pigs, the effects of γ‐aminobutyric acid (GABA) and GABAmimetic drugs have been investigated on tracheal segments contracted by cumulative application of an allergen (ovoalbumin, OA) and on serosal mast cells. The same drugs have also been tested on activation of alveolar macrophages isolated from unsensitized guinea‐pigs. Superfusion with GABA (1–1000 μM) reduced the contraction intensity of tracheal strips. The effect of GABA (100 μM) was not affected by the carrier blockers, nipecotic acid and β‐alanine (300 μM each). It was mimicked by the GABAB agonist (−)−baclofen (100 μM) but not 3‐aminopropanephosphinic acid (100 μM, 3‐APA). The GABAA agonist, isoguvacine (100 μM) did not exert any effect. GABA (10 μM)‐induced inhibition of tracheal contractions was reduced by the GABAB antagonist, 2‐hydroxysaclofen (100 μM, 2‐HS), but not by the GABAA antagonist, bicuculline (30 μM). The reduction in contraction intensity induced by GABA (100 μM) was prevented by a 40 min preincubation of tracheal strips with capsaicin (10 μM), but not tetrodotoxin (TTX, 0.3 μM). The effect of GABA (1000 μM) was absent after preincubation with indomethacin (2.8 μM) but unmodified when nordihydroguaiaretic acid (NDGA, 3.3 μM) was used. Finally, removal of the epithelium prevented the GABA effect. Anaphylactic histamine release from serosal mast cells isolated from sensitized animals was not affected either by GABA (10–1000 μM) or the selective receptor agonists (−)−baclofen (0.1–1000 μM) and isoguvacine (10–1000 μM). The release of platelet‐activating factor (PAF) from alveolar macrophages stimulated by formyl‐Met‐Leu‐Phe (FMLP; 1 μM) was modified neither by GABA (100 μM) nor by (−)−baclofen (100 μM). In conclusion, these data show that GABA can inhibit allergic phenomena in the guinea‐pig airways through activation of GABAB receptors. An involvement of neuropeptidergic sensory structures is suggested but a role for epithelial cells and arachidonate metabolites is not definitely proved.

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Section: Discussionsupporting

confidence: 84%

GABA‐mediated inhibition of the anaphylactic response in the guinea‐pig trachea

Gentilini

Franchi‐Micheli

Mugnai

et al. 1995

British J Pharmacology

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“…One component of the inflammatory response to bradykinin is increased microvascular leakage of plasma proteins in a number of tissues, including the airways (Saria et al, 1983). The mechanism of action of bradykinin in inducing airway leakage has not, however, been determined but may be via activation of several secondary mechanisms.…”

Section: Introduction Methodsmentioning

confidence: 99%

“…Leakage of Evans blue dye was determined in response to i.v. bradykinin at concentrations in the range 0.094-940 nmol kg-1 (Saria et al, 1983). At time 0, 1 ml kg-saline was given i.v.…”

Section: Experimental Protocolmentioning

confidence: 99%

Bradykinin‐induced plasma exudation in guinea‐pig airways: involvement of platelet activating factor

Rogers

Dijk

Barnes

1990

British J Pharmacology

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1 We studied the effect of bradykinin on plasma exudation in the airways of the anaesthetized guineapig in vivo. Tissue content of extravasated Evans blue dye was used as an index of protein exudation in the larynx, trachea, main bronchi and intrapulmonary airways (i.p.a.). 2 Bradykinin increased the content of Evans blue in all tissues studied in a dose-related manner. The response was greatest in the main bronchi and i.p.a., less in the trachea and least in the larynx. A dose of 47 nmol kg-1 was the lowest tested which caused significant (P < 0.001) plasma exudation with increases in leakage above control values of 256% in the larynx, 405% in the trachea, 394% in the main bronchi and 485% in intrapulmonary airways. 3 Leakage was significantly (P < 0.05) increased above control values by 1 min after bradykinin (47nmol kg-1) in the main bronchi and intrapulmonary airways and was maximal in all airways 5min after bradykinin. Although reduced by 15min, the tissue content of dye was still significantly (P < 0.05) increased 2 h after bradykinin. 4 The prolonged tissue dye retention was due to a later phase of slow and maintained exudation preventing full clearance of dye after the initial response. 5The initial phase of leakage was partially attenuated by the platelet activating factor (PAF) receptor antagonists WEB 2086 or BN 52021, by indomethacin or by inhibiting sensory nerve activation by opioid anaesthesia: it was not affected by mepyramine and cimetidine nor by the sulphidopeptide leukotriene receptor antagonists FPL 55712 or ICI 198,615. Adrenoceptor blockade of the anti-leakage effects of endogenously-released catecholamines significantly (P < 0.05) enhanced leakage. 6 The later phase of plasma leakage was completely inhibited by the PAF antagonists. 7 We conclude that, in guinea-pig airways in vivo, the initial phase of bradykinin-induced plasma exudation is mediated in part by PAF, sensory nerves and prostaglandins, whereas the later, prolonged phase of leakage is mediated exclusively by PAF. If bradykinin is generated in asthma, its potent and prolonged effects on plasma leakage may contribute significantly to airway oedema and may be involved in the development of bronchial hyperresponsiveness.

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“…Há outros corantes, além do azul de Evans, que se ligam à albumina, como o azul Celeste de Niágara, o azul Celeste de Pontamina 6BX e o azul de Tripan (2,(10)(11)(12)(13)(14)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29) . O azul de Evans é um corante capaz de ser mensurável por meio de espectrofotometria (11)(12) .…”

Section: Introductionunclassified

Avaliação espectrofotométrica do azul de Evans na reação inflamatória da córnea: estudo experimental em coelhos

Gehlen¹,

Moreira²,

Moreira³

et al. 2004

Arq. Bras. Oftalmol.

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Avaliação espectrofotométrica do azul de Evans na reação inflamatória da córnea: estudo experimental em coelhosObjetivo: Constatar a presença do azul de Evans na córnea normal estipulando o período de tempo de concentração máxima do corante após inoculação endovenosa e estudar a permeabilidade vascular em modelo animal da inflamação corneal induzida por queimadura química por meio de injeção de azul de Evans. Métodos: Cinquenta coelhos foram divididos em 3 grupos: Grupo I (25 animais): injetou-se 20 mg/kg de azul de Evans e os animais foram sacrificados após 8, 10, 12, 14 e 16 horas. Retirou-se a córnea e quantificou-se o corante por meio de micrométodo espectrofotométrico. Grupo II: em 15 animais injetou-se o corante e, após 10 horas, fragmentouse centralmente o tecido com trépanos de 6, 8 e 10 mm. Procedeu-se à extração do azul de Evans da mesma forma que no grupo I. Grupo III: induziu-se queimadura na córnea do olho direito de 10 animais com NaOH a 1 N. Cinco dias após o procedimento, os animais foram sacrificados, sendo que, 10 horas antes do sacrifício, foi inoculado o azul de Evans para que posteriormente se pudesse quantificá-lo. A córnea esquerda serviu como controle. Resultados: No grupo I, a média da concentração do azul de Evans às 10 h. foi de 15,28 ± 0,09 µg/mg. No grupo II, as médias das concentrações do corante foram: 6 mm: 0,93 ± 0,01µg/mg; 8 mm: 1,20 ± 0,06 µg/mg; 10 mm: 1,32 ± 0,05 µg/mg. No grupo III, as médias das concentrações do azul de Evans foram: olho direito (queimadura): 23,74 ± 2,64 µg/mg e olho esquerdo (controle): 16,71 ± 2,04 µg/mg. Conclusões: Quantificou-se o azul de Evans pela primeira vez na córnea de coelhos e constatou-se que, após 10 horas de inoculação endovenosa, o corante atingiu seu pico de concentração no tecido. Concluiu-se que o azul de Evans serve como bom método de quantificação da permeabilidade vascular alterada na córnea de coelhos. INTRODUÇÃODesde 1943, com os primeiros estudos de Rawson, o azul de Evans tem sido amplamente utilizado em diversos trabalhos experimentais. Este corante apresenta algumas características como inocuidade (1)(2) , alta solubilidade em água e afinidade pela albumina (3)(4)(5) . O azul de Evans, quando inoculado via endovenosa, combina-se com a albumina de maneira reversível e dependente de pH (4) .Estudos demonstraram que, após 40 horas da administração endovenosa do azul de Evans em ratos, 90% do corante já havia deixado a circulação, atingindo diversos tecidos do organismo. Depois de 24 horas de inoculação

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Vascular protein leakage in various tissues induced by substance P, capsaicin, bradykinin, serotonin, histamine and by antigen challenge

Cited by 410 publications

References 28 publications

GABA‐mediated inhibition of the anaphylactic response in the guinea‐pig trachea

GABA‐mediated inhibition of the anaphylactic response in the guinea‐pig trachea

Bradykinin‐induced plasma exudation in guinea‐pig airways: involvement of platelet activating factor

Avaliação espectrofotométrica do azul de Evans na reação inflamatória da córnea: estudo experimental em coelhos

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