Processes and bronchial hyperresponsiveness.
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Adenosine↗
Biomedical subjects
J Kips
Publications and source records attributed to J Kips.
Airway hyperreactivity, an introduction.
Asthma is characterized by the presence of airway inflammation and an increased responsiveness to many different stimuli. The hyperresponsiveness to indirect stimuli such as adenosine, bradykinin, neuropeptides, sulphur dioxide suggest that the hyperresponsiveness in asthma results from the complex interaction between inflammatory cells, neurons and smooth muscle cells. Several mechanisms may be involved in the influence of airway inflammation on airway responsiveness: increased mucosa permeability: enhanced exposure of irritant receptors, modulation of airway smooth muscle behavior by inflammatory mediators, mucosal edema, enhanced release of neurotransmitters, increased local reflex activity, decreased breakdown of neurotransmitters, etc. We have investigated the interaction between airway inflammation and responsiveness in two animal models: acute exposure to endotoxin and chronic exposure to aerosolized antigen. Both models demonstrate the complexity of interaction between inflammatory processes and demonstrate positive controlling mechanisms that inhibit the increase in airway responsiveness due to airway inflammation. The lack of such controlling mechanisms may be involved in the development of the asthmatic airway hyperresponsiveness.
Administration, Inhalation↗
Interactions between neurotransmitters and inflammatory cells in the airways.
Neuropeptides and purines are possible autonomic neurotransmitters. Both tachykinins (neurokinin A, substance P) and adenosine cause acute airway narrowing by synergistic activation of airway mast cells and postganglionic vagal nerve endings.
Adenosine↗
[Severe methanol poisoning].
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Acid-Base Equilibrium↗
The effect of tachykinins on the conducting airways of the rat.
We studied the bronchial effects of intravenously administered tachykinins in inbred rats. Substance P and related tachykinins caused a dose-dependent bronchoconstriction. The bronchial reactivity to substance P differed significantly between different inbred rat strains. Substance K, eledoisin and kassinin were more potent than substance P in causing bronchoconstriction. This suggests a predominance in the bronchi of SP-E receptors. The bronchial effects of substance P and eledoisin were largely inhibited by atropine and slightly enhanced by hexamethonium. In addition to a direct effect on airway smooth muscle, tachykinins interfere with the cholinergic airway innervation of the rat at the ganglionic and postganglionic level.
Airway Resistance↗
The respiratory effects of neuropeptides.
Several peptides have been localised to pulmonary nerves and endocrine cells. The neuropeptides vasoactive intestinal polypeptide (VIP) and substance P have potent effects on the airway smooth muscle, bronchial glands and blood vessels. There is increasing evidence that VIP and substance P are neurotransmitters of the non-adrenergic, non-cholinergic nervous (NANC) system. Non-adrenergic inhibitory nerves are the predominant inhibitory nervous system of the human airways. The presence of VIP in the innervation of the airways and the demonstration that it can mimick the effect of NANC nerve stimulation supports the hypothesis that it could be a mediator of the NANC system in the lungs. Sensory nerve fibers containing substance P can contribute to the smooth muscle contraction and mucosal oedema seen in asthma, by local axon reflexes that are initiated by noxious stimuli, such as for example cigarette smoke. A rat model for study of the bronchial reaction to substance P and related tachykinins, is described. In addition to a direct effect on airway smooth muscle, a large part of the broncho-constrictory actions of tachykinins in the rat is mediated by interaction with cholinergic nerves.
Airway Resistance↗
Synergistic mechanisms in the adenosine- and neuropeptide-induced bronchoconstriction.
Neuropeptides and purines are possible neurotransmitters of the nonadrenergic noncholinergic nervous system of the airways. We investigated possible synergistic mechanisms between these two bronchoconstricting agents in a rat model. We observed that both adenosine and tachykinins enhance histamine release in the airways and that adenosine and neurokinin A act synergistically both on airway narrowing and histamine release.
Acetylcholine↗