Involvement of tachykinins in pentamidine-induced airway constriction and microvascular leakage in the guinea pig.

  title={Involvement of tachykinins in pentamidine-induced airway constriction and microvascular leakage in the guinea pig.},
  author={Pierre Henri Jarreau and A. Harf and Micheline Levame and V Boyer and Hubert Lorino and Isabelle Macquin‐Mavier},
  journal={The American review of respiratory disease},
  volume={147 6 Pt 1},
We investigated the effects of aerosolized pentamidine isethionate on airway constriction and microvascular leakage in the guinea pig, and the role of tachykinins in these abnormalities. The bronchoconstrictor response to pentamidine was determined in anesthetized, tracheotomized and mechanically ventilated guinea pigs by exposing them to increasing concentrations of aerosolized pentamidine (5 to 30 mg/ml; 60 breaths). Respiratory system resistance was measured by the occlusion method. Airway… 

Aerosolized tachykinin antagonists inhibit pentamidine‐induced bronchoconstriction in guinea pigs

It is demonstrated that in the guinea pig, pentamidine‐induced bronchoconstriction is mediated through both NK1 and NK2 tachykinin‐receptor activation and that when directly administered into the airways, tachy Kinin antagonists effectively prevent pentamazine‐induced BronchoconStriction.

An important role of tachykinins in ozone-induced airway hyperresponsiveness.

Results suggest that tachykinins may be responsible for ozone-induced AHR, possibly via neurogenic inflammation, in guinea pigs as well as vehicle-pretreated animals.

Indirect muscarinic receptor activation by pentamidine on airway smooth muscle

The overall results suggest that pentamidine induces contraction of guinea‐pig and human isolated bronchi through prejunctional cholinergic nerve stimulation.

The effects of a specific tachykinin receptor antagonist FK‐224 on ozone‐induced airway hyperresponsiveness and inflammation

It is concluded that neurogenic inflammation caused by tachykinin release may be responsible for ozone‐induced bronchial hyperresponsiveness, and that tachy Kinins may play a role in the initiation of airway inflammation.

Neurokinin mediation of edema and inflammation

The involvement of SP, NKA and NKB is examined in relation to the major signs of inflammation, including edema formation, protein plasma extravasation and vasodilatation, as well as to the receptor subtypes involved in neurokinin-mediated inflammation.



Effect of antiasthma drugs on microvascular leakage in guinea pig airways.

The results suggest that the antiedema effect of epinephrine may be due to vasoconstriction rather than to a direct effect on endothelial cell contractility and that neither beta-agonists nor theophylline have an inhibitory effect.

Effects of neuraminidase on airway reactivity in the guinea pig.

Results indicate that in the guinea pig, neuraminidase injected intratracheally does not induce non-specific airway hyperreactivity and may alter the binding of substance P to its receptors.

Bronchoconstriction induced by inhaled sodium metabisulfite in the guinea pig. Effect of capsaicin pretreatment and of neutral endopeptidase inhibition.

The data demonstrate that inhaled MBS causes bronchoconstriction in guinea pigs by mechanisms that are due neither to a cholinergic reflex nor to the release of tachykinins from airway sensory nerves.

Substance P-induced bronchoconstriction in the guinea pig. Enhancement by inhibitors of neutral metalloendopeptidase and angiotensin-converting enzyme.

The data suggest that conditions associated with diminished peptidase activity could result in enhanced responses to stimuli which cause the release of endogenous substance P, and degrade of substance P by both NEP and ACE is important for determining the magnitude of the bronchoconstriction caused by intravenous administration of this peptide.

Formoterol and salbutamol inhibit bradykinin‐ and histamine‐induced airway microvascular leakage in guinea‐pig

In conclusion, intravenously injected β‐adrenoceptor stimulants can inhibit, partially or totally, the increase of airways microvascular permeability induced by intravenous histamine or bradykinin, however, these effects require doses that inhibit the increase in pulmonary airway resistance induced by these mediators.

Influence of body temperature on histamine-induced bronchoconstriction in guinea pigs.

The results suggest that, at low body temperatures, increased airway responsiveness to histamine may be because of some direct effect of temperature on bronchial airway smooth muscle.

Neurogenic plasma extravasation: inhibition by morphine in guinea pig airways in vivo.

It is concluded that morphine inhibits neurogenic plasma leakage by presynaptic inhibition of release of neuropeptides from sensory nerve endings by opioid drugs devoid of central effects may be of value in the therapy of asthma.

Airway neutral endopeptidase-like enzyme modulates tachykinin-induced bronchoconstriction in vivo.

To determine whether neutral endopeptidase (NEP), also called enkephalinase (EC, modulates the effects of exogenous and endogenous tachykinins in vivo, it was found that NEP-like activity in tracheal homogenates of guinea pig was inhibited by phosphoramidon.

Selective delivery of pentamidine to the lung by aerosol.

In 8 patients with diffuse infiltrates on chest radiograph undergoing fiberoptic bronchoscopy for suspected Pneumocystis carinii pneumonia, bronchoalveolar lavage sediment and supernatant

Comparison of tissular disposition of pentamidine mesylate in the rat after aerosol or parenteral administration.

The tissular distribution of pentamidine mesylate (4 mg/kg as free base) after intravenous, intramuscular, and aerosol administration in healthy rats was examined. Pentamidine levels in the plasma,