Modulatory effect of neuropeptide Y on acetylcholine‐induced oedema and vasoconstriction in isolated perfused lungs of rabbit

@article{Delaunois1994ModulatoryEO,
  title={Modulatory effect of neuropeptide Y on acetylcholine‐induced oedema and vasoconstriction in isolated perfused lungs of rabbit},
  author={Annie Delaunois and Pascal Gustin and Cécile Dessy-Doizé and Michel Ansay},
  journal={British Journal of Pharmacology},
  year={1994},
  volume={113}
}
1 The modulatory role of neuropeptide Y (NPY) on pulmonary oedema induced by acetylcholine and capsaicin was investigated. The effects of NPY on the haemodynamic response to acetylcholine, phenylephrine and substance P were also investigated. 2 Isolated, ventilated, exsanguinated lungs of the rabbit were perfused with a constant flow of recirculating blood‐free perfusate. The double/arterial/venous occlusion method was used to partition the total pressure gradient (ΔPt) into four components… 

Effect of neuropeptide Y on hemodynamics of the rabbit lung.

Although NPY is a potent vasoconstrictor in the rabbit lung, it is not likely that plasma NPY concentrations rise sufficiently, even after massive sympathetic nervous system activation, to produce pulmonary vasoconStriction in the intact rabbit.

Interactions between acetylcholine and substance P effects on lung mechanics in the rabbit

It is concluded that ACh‐induced changes in lung resistance and compliance are in part mediated by a direct effect on airway smooth muscle and in part by the stimulation of C fibers, by the release of histamine from mast cells and by the synthesis of arachidonic acid metabolites.

Interactions between cytochrome P-450 activities and ozone-induced modulatory effects on endothelial permeability in rabbit lungs: influence of gender.

It was concluded that inhibition of 2 different CYP450-dependent activities after exposure to 0.4 ppm O(3) for 4 h appears to be a gender-dependent phenomenon, and that CYP 450 is probably involved in the O( 3)-evoked inhibitory mechanism against ACh-induced increase in endothelial permeability, but only in males.

Ozone-induced stimulation of pulmonary sympathetic fibers: a protective mechanism against edema.

Using a model of permeability edema in isolated perfused rabbit lungs, it is reported that, immediately after exposure of rabbits to 0.4 ppm ozone for 4 hr, the pulmonary microvascular responses to acetylcholine and substance P are completely blocked, resulting in transient protection against pulmonary edema.

Non-neuronal neuropeptide Y and its receptors during acute rejection of rat pulmonary allografts.

Role of Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) in Modulating Vascular Smooth Muscle Cells by Activating Large-Conductance Potassium Ion Channels

Evidence that the K+ channels are modulated by a direct action of non-steroidal antiinflammatory drugs (NSAIDs) to activate the K- ion channels is presented.

Comparison of ozone-induced effects on lung mechanics and hemodynamics in the rabbit.

It is concluded that O3 can induce direct vascular constriction and inhibit the ACh-, SP-, and histamine-induced changes in lung mechanical properties.

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