Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Protection of the lungs against ventilator-induced lung injury is becoming one of the main concerns in pediatric and neonatal intensive care. High frequency ventilation using a constant distending pressure with small variations during respiratory cycles allows adequate recruitment. High frequency oscillation is the most promising HFV mode especially in premature neonates but clinical studies are contradictory. Nitric oxide, an inhaled gas with specific pulmonary vasodilating effects, has become a powerful tool in the treatment of pulmonary arterial hypertension alone or in combination with HFO, but studies have failed to show improvement in survival in neonates as well as in children with ARDS. Tracheal gas insufflation, in addition to conventional ventilation, by washing dead space during exhalation, improves gas exchange while lowering tidal volume. It is however still experimental. Maintenance of spontaneous ventilation during conventional ventilation improves gas exchange, hemodynamic functions, mobilization, active coughing, and avoids prolonged muscle weakness. Non invasive modes of ventilation like BiPAP have certain indications in pediatrics but need to become more familiar to the pediatric intensivist.
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PMID:New tools in ventilatory support: high frequency ventilation, nitric oxide, tracheal gas insufflation, non-invasive ventilation. 1009 36

The human airways are innervated via efferent and afferent autonomic nerves, which regulate many aspects of airway function. It has been suggested that neural control of the airways may be abnormal in asthmatic patients, and that neurogenic mechanisms may contribute to the pathogenesis and pathophysiology of asthma. In this review, the autonomic innervation of the human airways and possible abnormalities in asthma are discussed. The parasympathetic nervous system is the dominant neuronal pathway in the control of airway smooth muscle tone. Stimulation of cholinergic nerves causes bronchoconstriction, mucus secretion, and bronchial vasodilation. Although abnormalities of the cholinergic innervation have been suggested in asthma, thus far the evidence for cholinergic dysfunction in asthmatic subjects is not convincing. Sympathetic nerves may control tracheobronchial blood vessels, but no innervation of human airway smooth muscle has been demonstrated. beta-Adrenergic receptors, however, are abundantly expressed on human airway smooth muscle and activation of these receptors causes bronchodilation. The physiological role of beta-adrenergic receptors is unclear and their function seems normal in asthmatic patients. Inhibitory nonadrenergic noncholinergic (NANC) nerves, containing vasoactive intestinal peptide and nitric oxide, may be the only neural bronchodilator pathways in human airways. Although a dysfunction of inhibitory NANC nerves has been proposed in asthma, thus far no differences in inhibitory NANC responses have been found between asthmatics and healthy subjects. Excitatory NANC nerves, extensively studied in animal airways, have also been detected in human airways. In animal studies, stimulation of excitatory NANC nerves causes bronchoconstriction, mucus secretion, vascular hyperpermeability, cough, and vasodilation, a process called 'neurogenic inflammation'. Recent studies have demonstrated an interaction between the excitatory NANC nervous system and inflammatory cells. Neuropeptides may influence the recruitment, proliferation, and activation of leukocytes. On the other hand, inflammatory cells may modulate the neuronal phenotype and function. The functional relevance of the excitatory NANC nervous system and its interaction with the immune system in asthma still remains to be elucidated.
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PMID:Autonomic innervation of human airways: structure, function, and pathophysiology in asthma. 1021 12

Normobaric oxygen toxicity is well described in all animal species. However susceptibility to oxygen exposure is highly variable according to age, species and strains. Similarly in humans, prolonged high oxygen exposure is reported to induce cough, shortness of breath, decrease vital capacity and increase alveolo-capillary permeability. The toxic FIO2 threshold (length of exposure and level) is still debated. In patients with previous lung injury, this threshold is even more difficult to delineate as pathologic pulmonary lesions might result from hyperoxia or primary lung insult. Oxygen free-radicals play a key role in the pathophysiology of oxygen toxicity. Oxygen resistance or tolerance is obtained with intraperitoneal, intravenous and intratracheal endotoxin or cytokines administration. Previous exposure to high oxygen concentration is also reported to increase survival rate and decrease pulmonary lesions in animal models. Protection may rely on antioxidant enzymes synthesis, nitric oxide production, neutrophils recruitment and modulation of alveolar macrophages activity. In humans, oxygen tolerance might be suspected through several clinical studies reporting favorable outcome after long term-oxygen exposure. Better knowledge of the risks of prolonged high oxygen exposure is important to re-evaluate the goals of mechanical ventilation (FIO2, SaO2, PEEP) and/or to develop treatments to prevent oxygen toxicity (surfactant, antioxidant enzymes).
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PMID:Oxygen toxicity and tolerance. 1039 7

Epidemiological data indicate that living or working in a moldy building is associated with increased risk of respiratory symptoms and disease related to inflammatory reactions, but biochemical evidence linking cause and effect is still scarce. The staff working in a mold-contaminated school, and a reference group without such exposure, were studied. Nasal lavage was performed and health data were collected with a questionnaire at the end of the spring term, after a 2.5-mo summer vacation, and at the end of the fall term. Here we show that concentrations of tumor necrosis factor alpha (TNF-alpha), interleukin-6 (IL-6), and nitric oxide (NO) in nasal lavage fluid were significantly higher in the exposed than in the control subjects at the end of the first exposure period. These inflammatory mediators decreased to reference group concentrations during the period when there was no exposure and the production of NO and IL-6 increased again during the reexposure in the fall term. Reports of cough, phlegm, rhinitis, eye irritation, and fatigue paralleled the changes in the measured inflammatory markers. These results point to an association between inflammatory markers in the nasal lavage fluid, the high prevalence of respiratory symptoms among the occupants, and chronic exposure to molds in the indoor environment.
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PMID:Nitric oxide and proinflammatory cytokines in nasal lavage fluid associated with symptoms and exposure to moldy building microbes. 1058 10

Primary ciliary dyskinesia (PCD) is an inherited condition characterised by functional and/or structural congenital abnormalities of cilia. Presentation is often in the neonatal period, but there are age-related differences in presentation, and diagnosis is often delayed. The usual clinical picture is of recurrent upper and lower respiratory symptoms (rhinitis, glue ear, recurrent cough and sputum production), with mirror image arrangement in 50% of the children. Around 50% males have immotile sperm, but male infertility is not invariable. There are known associations between PCD and complex congenital heart disease, severe oesophageal disease, and more rarely, hydrocephalus and biliary atresia. Diagnosis is with a combination of the saccharine test, nasal nitric oxide, ciliary beat frequency and electron microscopy. Patients should be followed up by specialists familiar with the different ways of managing the upper and lower airway complications.
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PMID:Primary ciliary dyskinesia. 1108 68

We report a rare case of acute respiratory distress syndrome (ARDS) induced by Influenza A (H3 N2) without secondary microbiological infection. A 69-year-old woman was admitted to our hospital because of cough and severe dyspnea. We diagnosed ARDS, because of the severe respiratory failure resistant to high-dose oxygen, the diffuse bilateral infiltrates without cardiomegaly on chest radiography, and the normal pulmonary artery wedge pressure. This patient was treated with high doses of methylprednisolone, antibiotics, globulins, urinastatin, neutrophilic elastase inhibitor, nitric oxide inhalation, and extracorporeal membrane oxygenation, but died on the thirteenth hospital day. Our final diagnosis was ARDS induced by fulminant influenza (A/Hong Kong/68 (H3 N2)) virus pneumonia, because the antibody titers of H3 N2 influenza of paired sera showed a 128-fold increase.
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PMID:[A case of acute respiratory distress syndrome induced by fulminant influenza A (H3 N2) pneumonia]. 1118 25

In asthma patients, microaspiration of acid into the lower airways (ie, airway acidification) causes such respiratory responses as cough and bronchoconstriction. The mechanism of bronchoconstriction induced by airway acidification is unknown, although evidence is emerging that increasing proton concentrations in airway tissues can activate a subpopulation of primary sensory neurons, so-called capsaicin-sensitive primary sensory neurons, that contain such neuropeptides as the tachykinins substance P (SP) and neurokinin A (NKA). Protons activate a capsaicin-operated channel/receptor, located in the afferents of capsaicin-sensitive neurons, with the subsequent opening of ion channels that are permeable to sodium, potassium, and calcium ions. This event initiates a propagated action potential that antidromically depolarizes collateral fibers and triggers neuropeptide release from nerve fiber varicosities. The tachykinins SP and NKA, released from terminals of primary sensory neurons in peripheral tissues, cause all the major signs of inflammation (neurogenic inflammation) by means of activation of NK(1) and NK(2) receptors. Exposure of the airways to acidic solutions stimulates sensory nerve endings of capsaicin-sensitive sensory neurons and causes different airway responses, including bronchoconstriction. Recently, the NK(2), and to a lesser extent the NK(1), receptors have been shown to be involved with citric acid-induced bronchoconstriction in the guinea pig, which is in part mediated by endogenously released bradykinin. Tachykinins and bradykinin, released by airway acidification, could also modulate citric acid-induced bronchoconstriction by their ability to subsequently release the epithelially derived bronchoprotective nitric oxide (NO). Further study with selective tachykinin NK(1) and NK(2) agonists demonstrated that only the septide-insensitive tachykinin NK(1) receptor releases NO. Thus, bronchoconstriction induced by citric acid inhalation in the guinea pig, mainly caused by the tachykinin NK(2) receptor, is counteracted by bronchoprotective NO after activation of bradykinin B(2) and tachykinin NK(1) receptors in airway epithelium. If a similar mechanism is involved in the pathogenesis of bronchial asthma associated with gastroesophageal reflux in the respiratory tract, new therapeutic strategies should be investigated.
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PMID:Mechanisms of citric acid-induced bronchoconstriction. 1174 19

Because many antihypertensive drugs can affect airway function, the treatment of hypertension in patients with airway dysfunction is complex. For example, the worsening or precipitation of asthma by beta-adrenoceptor antagonists is well-recognized, but beta(1)-adrenoceptor blockers that exert mild beta(2)-agonist effects, and those that modulate the endogenous production of nitric oxide, affect airway function to a lesser extent. Therapy with selective alpha(1)-blockers is not contraindicated in cases of chronic airway obstruction. Conversely, alpha(2)-agonists must not be given to asthmatic subjects because they can adversely affect the bronchi. Calcium channel blockers do not exert severe side effects on the airways. Angiotensin-converting enzyme inhibitors may cause cough and exacerbate or even induce asthma; however, angiotensin II type I (AT(1)) antagonists do not cause cough. 5-Hydroxytryptamine modifiers such as urapidil are a treatment option for patients with chronic airway obstruction. In patients with airway dysfunction, we suggest treatment with thiazide diuretics as the initial drug choice, and calcium channel blockers if the response is poor. In the case of no response, calcium channel blockers alone must be used. However, there is no strict rule because individual patients may respond differently to individual drugs and drug combinations. Consequently, it is important to adopt a flexible approach. For patients who are unresponsive to the aforementioned drugs, AT(1) receptor antagonists, newer beta(1)-adrenoceptor-blocking agents with ancillary properties (eg, celiprolol or nebivolol), and/or vasodilators can be considered.
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PMID:The pharmacologic treatment of uncomplicated arterial hypertension in patients with airway dysfunction. 1179 56

The herb, Chrysanthemum zawadskii var, latilobum commomly known as Gu-Jul-Cho in Korea, used in traditional medicine to treat pneumonia, bronchitis, cough, common cold, pharyngitis, bladder-related disorders, gastroenteric disorders, and hypertension. Linarin is the main active compound and the biological mechanisms of its activity are unclear. It is believed that effects of this herb may be exerted through the pluripotent effectors of linarin due to its ability to treat a variety of afflictions. In this study, the effects of linarin on the mouse macrophages cell line, RAW 264.7, were investigated. It was found that linarin could activate macrophages by producing cytokines. Monocytes and tissue macrophages produce at least two groups of protein mediators of inflammation, interleukin 1 (IL-1) and the tumor necrosis factor (TNF). Recent studies have shown that TNF and IL-1 modulate the inflammatory function of endothelial cells, leukocytes, and fibroblasts. TNF-alpha production by macrophages treated with linarin occured in a dose dependent manner. However, IL-1 production was largely unaffected by this natural product. This study demonstrated the ability of linarin to activate macrophages both directly and indirectly. Linarin also affect both cytokine production and nitric oxide inhibition, in addition to the expression of some surface molecules. Nitric oxide (NO), derived from L-argin-ine, is produced by two forms(constitutive and inducible) of nitric oxide synthase (NOS). The NO produced in large amounts by inducible NOS is known to be responsible for the vasodilation and hypotension observed in septic shock. Linarin was found to inhibit NO production in the LPS-activated RAW 264.7 cells. Linarin may be a useful candidate as a new drug for treating endotoxemia and the inflammation accompanied by NO overproduction. The linarin-treated total lymphocytes exhibited cytotoxicity in a dose dependent manner between 20 microg/ml and 40 microg/ml. These results suggest that linarin may function through macrophage activation.
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PMID:The effect of linarin on LPS-induced cytokine production and nitric oxide inhibition in murine macrophages cell line RAW264.7. 1200 31

1. Bradykinin (BK) is a nine amino acid peptide (Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg) formed from the plasma precursor kininogen during inflammation and tissue injury. The actions of BK are mediated by G protein-coupled cell surface receptors, designated B1 and B2. 2. BK has a plethora of effects in the airways including bronchoconstriction, bronchodilation, stimulation of cholinergic and sensory nerves, mucus secretion, cough and oedema resulting from promotion of microvascular leakage. These airway effects are mediated in the main by the B2 receptor subtype. 3. BK acts mainly indirectly, primarily through airway nerve activation, but also by the release of prostanoids, thromboxanes and nitric oxide (NO). 4. Airway responses to BK have been studied in detail in guinea-pigs, mice, sheep and rats. This review describes the effects of BK in these species and draws comparison with its effects in normal humans and patients with respiratory diseases. 5. Despite its many and varied effects in the airways of animals and man, the exact contribution of BK to airways disease remains unclear.
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PMID:Species differences in bradykinin receptor-mediated responses of the airways. 1242 22


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