Modulation of neurally mediated airway microvascular leakage in guinea-pig airways byβ 2 agonists

Hui, K P; Ventresca, Pietro; Brown, A. C.; Barnes, Peter J.; Chung, Kian Fan

doi:10.1007/bf01991224

Cited by 9 publications

(7 citation statements)

References 11 publications

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“…fl2-adrenoceptor agonists have been shown to attenuate airway microvascular leakage induced by various mediators such as histamine [3][4][5] and bradykinin [3,5,6]. In addition, inhibition of neurogenic-induced airway microvascular leakage has been reported [3,7,8]. The effect of fl2-adrenoceptor agonists in preventing bronchoconstriction appears to be more potent than in reducing airway microvascular leakage as shown against histamine-induced effects [4].…”

Section: Introductionmentioning

confidence: 89%

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Effect ofβ(in2)-adrenoceptor agonists against platelet-activating factor-induced airway microvascular leakage and bronchoconstriction in the guinea pig

Sakamoto¹,

Barnes²,

Chung³

1993

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We have investigated the effect of inhaled formoterol (0.75 mg/ml, 60 breaths) and salbutamol (25 mg/ml, 60 breaths) against airway microvascular leakage and bronchoconstriction induced by inhaled platelet-activating factor (PAF) and histamine in anaesthetized guinea pigs. Lung resistance (RL) was measured for 6 min after challenge, followed by measurement of extravasation of Evans blue dye into airway tissues, used as an index of airway microvascular leakage. PAF (0.1, 0.4 and 1 mM; 30 breaths) caused a significant increase in RL and extravasation of dye, but the responses were smaller than those induced by histamine (5 mM, 30 breaths). Both formoterol and salbutamol caused a small but significant inhibition of extravasation in the distal intrapulmonary airways induced by PAF (0.1 and 0.4 mM for formoterol and 0.1 mM for salbutamol), and only formoterol reduced the increase in RL induced by 1 mM PAF. These drugs also inhibited both airway effects of histamine to a higher degree. In conclusion, formoterol and salbutamol can partly inhibit airway microvascular leakage and bronchoconstriction induced by inhaled PAF and histamine. The inhibitory potency of beta 2-adrenoceptor agonists may be dependent on the inflammatory mediator inducing the airway effects.

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Section: Introductionmentioning

confidence: 89%

“…We chose the doses of formoterol and salbutamol as previously used in a study in our laboratory [4]. PAF at the dose of 1 mM (30 breaths) has been shown to induce significant submaximal extravasation of Evans blue dye at all airway levels [8].…”

Section: Measurement Of Airway Microvascular Leakagementioning

confidence: 99%

Effect ofβ(in2)-adrenoceptor agonists against platelet-activating factor-induced airway microvascular leakage and bronchoconstriction in the guinea pig

Sakamoto¹,

Barnes²,

Chung³

1993

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“…Salbutamol completely inhibited the UNDW-induced increase in the Pao. It has been shown that intravenously administered salbutamol does not inhibit airway microvascular leakage induced by vagal stimulation [21], substance P [21], or platelet-activating factor [22], and that it has little or no inhibitory effect on histamine-induced microvascular permeability in proximal and distal intrapulmonary airways [23]. Taken together, it is likely that the increase in Pao is indicative of bronchoconstriction induced by the inhalation of UNDW in our guinea-pig model.…”

Section: Discussionmentioning

confidence: 62%

A guinea-pig model of ultrasonically nebulized distilled water-induced bronchoconstriction

Fujimura

Amemiya²,

Myou³

et al. 1997

Eur Respir J

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Ultrasonically nebulized distilled water-induced bronchoconstriction (UNDW-IB) is specific to asthma. The mechanisms underlying UNDW-IB are not fully understood, and no reproducible animal model has been reported. The purpose of this study was to develop a guinea-pig model of UNDW-IB. Ultrasonically nebulized distilled water (UNDW) was inhaled 20 min after an aerosolized antigen challenge in passively sensitized and artificially ventilated guinea-pigs. UNDW was also inhaled 5 and 20 min after 0.1 mg x mL(-1) methacholine inhalation in nonsensitized animals. In addition, 0.1 mg x kg(-1) S-1452, a thromboxane A2 antagonist, or saline was given intravenously 5 min before UNDW inhalation in sensitized animals. The inhalation of UNDW caused bronchoconstriction, when inhaled 20 min after an antigen challenge in sensitized guinea-pigs. UNDW inhalation did not produce bronchoconstriction after saline inhalation in nonsensitized or sensitized guinea-pigs, or after antigen inhalation in nonsensitized animals. Methacholine-induced bronchoconstriction did not evoke UNDW-IB. Neither did S-1452 reduce the UNDW-IB. In conclusion, the guinea-pig model of ultrasonically nebulized distilled water-induced bronchoconstriction developed in this study suggests that allergic reaction, but not bronchoconstriction, can induce bronchial hyperresponsiveness to ultrasonically nebulized distilled water, and that thromboxane A2 is not involved in ultrasonically nebulized distilled water-induced bronchoconstriction.

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“…Several mechanisms have been proposed for the anti-edema effects of 132 agonists. Amongthese mechanisms arethe inhibition of mastcell degranulation(6), a direct antipermeability action on the vascular endothelium (7), and the inhibition of inflammatory mediator release from sensory nerves (8,9).Formoterol is a new, potent, long-acting 132 agonistthat hasbeen shown to inhibit plasma extravasation in the airways caused by histamineand bradykinin (8, 10, 11), and by electrical stimulation …”

mentioning

confidence: 99%

mentioning

confidence: 99%

Anti-edema action of formoterol in rat trachea does not depend on capsaicin-sensitive sensory nerves.

Sulakvelidze

McDonald²

1994

Am J Respir Crit Care Med

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The beta 2-adrenergic agonist formoterol has been shown to inhibit plasma extravasation in the respiratory mucosa associated with neurogenic inflammation as well as that caused by histamine or bradykinin. It is unknown whether these effects of formoterol are mediated through an action of sensory nerves or through a direct effect on the leaky blood vessels. In the present study we sought to determine whether capsaicin-sensitive sensory nerves are essential for the anti-edema effect of formoterol in the rat trachea. Substance P (5 micrograms/kg), PAF (hexadecyl-PAF, 5 micrograms/kg), or bradykinin (10 mg/kg) was injected intravenously to increase vascular permeability. The amount of plasma extravasation was measured with two tracers, Evans blue dye and Monastral blue pigment. The effectiveness of formoterol's anti-edema action was assessed in two groups of rats. One was pretreated with capsaicin to eliminate tachykinin-containing sensory nerves and another, the control group, was not pretreated. We found that in control rats formoterol inhibited to a similar extent the extravasation of Evans blue and Monastral blue caused by all three mediators. The highest intravenous dose of formoterol (10 micrograms/kg) reduced substance P-induced extravasation of Monastral blue by 59%, reduced PAF-induced extravasation by 74%, and reduced bradykinin-induced extravasation by 58%. Pretreatment of rats with a dose of capsaicin that eliminated at least 94% of the substance P-immunoreactive nerve fibers did not significantly reduce the effectiveness of formoterol against any of the mediators.(ABSTRACT TRUNCATED AT 250 WORDS)

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Modulation of neurally mediated airway microvascular leakage in guinea-pig airways byβ 2 agonists

Cited by 9 publications

References 11 publications

Effect ofβ(in2)-adrenoceptor agonists against platelet-activating factor-induced airway microvascular leakage and bronchoconstriction in the guinea pig

Effect ofβ(in2)-adrenoceptor agonists against platelet-activating factor-induced airway microvascular leakage and bronchoconstriction in the guinea pig

A guinea-pig model of ultrasonically nebulized distilled water-induced bronchoconstriction

Anti-edema action of formoterol in rat trachea does not depend on capsaicin-sensitive sensory nerves.

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