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)

A 47 year old man with asthma, allergic rhinitis, and chronic maxillary and ethmoid sinusitis and polyposis, in whom for 2 years intraorbital pressure symptoms are experienced on nose-blowing, sneezing and coughing, is presented. Paranasal sinus X-rays demonstrated an intraorbital pneumocoele that increased in size with Valsalva manoeuvre. The diagnosis, pathology and treatment of intraorbital emphysema and pneumoceles are discussed.
HNO 1978 Oct
PMID:[Spontaneous ethmoid pneumocele in chronic maxillary and ethmoid sinusitis and polyposis (author's transl)]. 71 19

A solitary papilloma of the left main bronchus in a 48 year old man is described. The patient had a one year history of cough, hemoptysis and bronchospasm. Bronchoscopy and repeated removal of the tumour through the bronchoscope failed to control it, and local recurrence finally made pneumonectomy necessary.
HNO 1975 Jul
PMID:[Solitary bronchial papilloma (author's transl)]. 120 98

The laryngocele is a dilatation of the laryngeal ventricle and represents a rare condition. In most cases there is a typical history. Patients with an internal laryngocele usually complain of hoarseness, dyspnea and cough. Laryngoscopy shows a swelling of the false cord on one side. The external laryngocele presents as a swelling in the neck. In some cases the clinical presentation is not that typical, so that computed tomography (CT) can be a helpful, additional investigation. CT scans show either an air- or mucus-containing tumor at the level of the false cord. This internal laryngocele may proceed into an external one, which presents as a swelling at the level of the hyoid bone. We now present 13 cases of laryngoceles with special regard to the CT and intraoperative findings. In the differential diagnosis other tumors of the larynx are considered, since the mucus-filled laryngocele is difficult to distinguish.
HNO 1990 Jun
PMID:[Computerized tomography imaging of laryngocele. Its importance in the differential diagnosis of tumors of the larynx and pharynx]. 238 76

The larynx may be involved in patients with systemic sarcoidosis or may be the first or only manifestation of the disease. The symptoms depend on the degree of involvement of the larynx, and include a sensation of lump in the throat, dysphagia, hoarseness, cough, stridor and dyspnea. The supraglottis is the most frequently affected area. There are pale pink, edematous, diffuse hypertrophy of the supraglottic structures or granular areas of the glottic and subglottic region. The diagnosis is made by the characteristic appearance of the larynx, histologic and laboratory findings and exclusion of other granulomatous diseases. Laryngeal sarcoidosis may cause life-threatening upper airway obstruction. Systemic corticosteroid therapy is the treatment of choice in most cases, but surgical excision or local steroid injections are useful in selected cases.
HNO 1985 Mar
PMID:[Diagnosis and therapy of laryngeal sarcoidosis]. 399 72

Scorpion venoms contain specific toxins which block large conductance calcium-activated potassium (BKCa) channels. Use of these toxins has shown that a significant proportion of the action of bronchodilators such as beta-agonists, theophylline, and nitric oxide occurs as a result of the opening of BKCa channels. Similarly, these toxins have shown that inhibitors of airway neurotransmission also operate via BKCa channels. Drugs that open BKCa channels may be alternative bronchodilators (possibly "airway selective" and with fewer side effects) as well as inhibitors of pathophysiological neurogenic influences in asthma, chronic coughing and sneezing, and chronic bronchitis.
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PMID:Scorpion venoms: taking the sting out of lung disease. 871 88

There is much evidence that neural mechanisms are involved in the mechanisms and symptoms of asthma. Afferent nerves may be activated and sensitized by inflammatory mechanisms, resulting in symptoms such as cough and chest tightness, in activation of cholinergic reflexes and in the release of inflammatory neuropeptides. Cholinergic mechanisms are the predominant bronchoconstrictor neural pathway and may be enhanced in asthma, particularly during exacerbations, through several mechanisms, including impaired function of muscarinic autoreceptors on cholinergic nerve terminals. There may also be abnormalities in adrenergic control and in the function of beta-adrenoceptors, particularly in severe asthma. The neurotransmitter of bronchodilator nerves is now identified as nitric oxide and this mechanism may be impaired during asthma exacerbations. Finally, neurogenic inflammation, due to release of neuropeptides from sensory nerves, may contribute and amplify the inflammation in asthmatic airways.
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PMID:Overview of neural mechanisms in asthma. 878 68

Angiotensin receptor antagonists represent a new class of drugs for the treatment of patients with hypertension. Reduction of blood pressure in patients with essential hypertension requires increased activity of the renin-angiotensin system. Losartan, the first orally active, nonpeptide angiotensin antagonist, specifically competes with angiotensin II (Ang II) for the AT1 receptor and reversibly alters the receptor. Maximum blood pressure reductions occur after doses of approximately 50 mg, although some patients will require 100 mg; the parent compound and a metabolite are responsible for a smooth 24-hour effect on blood pressure. Once-daily dosing with losartan has been documented to be safe. The drug's safety has been evaluated in 4,058 patients; of these patients, more than 1,200 were treated for longer than 6 months and more than 800 were treated for longer than 1 year with doses of 10 mg to 150 mg. Overall, no hypertensive patients were withdrawn from treatment because of elevated serum creatinine or potassium levels, and there were no reports of angioedema. In addition, some reductions in plasma uric acid levels were noted. Cough occurred significantly less often in patients treated with losartan than in those treated with hydrochlorothiazide or lisinopril. In contrast to angiotensin-converting enzyme (ACE) inhibitors, losartan does not activate bradykinin-nitric oxide-prostanoid vasodilation.
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PMID:Losartan: first of a new class of angiotensin antagonists for the management of hypertension. 893 38

1. We tested the hypothesis that the pattern and the intensity of autonomic mechanisms causing vasoconstriction in the resting bronchial circulation of awake dogs also exists in awake sheep. It was also postulated that sighing behaviour and the associated bronchovascular dilatation induced by non-adrenergic, non-cholinergic (NANC) mechanisms observed in the dog exist in sheep. 2. Bronchial arterial blood flow to lower airways of both lungs of awake sheep was measured continuously using pulsed Doppler flow probes mounted on the bronchial artery at prior thoracotomy. 3. Cumulative and factorial analysis of responses to randomized combinations of autonomic alpha 1-, alpha 2-, beta 1- and beta 2-adrenoceptors and cholinoceptor autonomic blockade suggests that resting vasoconstrictor activity is less in sheep than in dogs. At normal aortic pressure, the autonomic activity of these receptor groups in the sheep lowers bronchial blood flow and conductance by 30%, whereas in the awake dog, the corresponding autonomic effect is 50%. 4. Tonic autonomic control of bronchial conductance can be partitioned in sheep to show significant and separate alpha- and beta-adrenoceptor vasoconstrictor activity at a ratio of 1.8:1, an effect normally offset by a weaker vasodilator alpha-/beta-adrenoceptor interaction. In contrast to the situation in awake dogs, cholinoceptors do not play a role in awake sheep. 5. Nitric oxide (NO) synthase inhibition in sheep using NG-nitro-L-arginine following blockade of alpha- and beta-adrenoceptors and cholinoceptors causes hypertension, but minor changes, if any, in pulmonary pressures or heart rate. Bronchial flow and conductance, however, fall from a higher resting conductance by approximately 50%, suggesting that, normally, resting bronchial flow conductance is dominated by strong tonic NO vasodilator effects that interact with weaker tonic autonomic vasoconstrictor effects. 6. Superimposed (respiratory) behaviours of sighing, sneezing and coughing, which involve negative swings in intrathoracic pressure and the movement of inspired air, evoke large active bronchovascular dilator effects. These appear to be largely NANC in origin and appear to be dependent, in part, on mechanisms associated with NO release. It is postulated that the C-fibre axon reflex using substance P, calcitonin gene-related peptide and neurokinin A may be involved. Vocalization and eructation do not evoke bronchovascular effects.
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PMID:Autonomic control of bronchial circulation in awake sheep during rest and behaviour. 940 60

Understanding the mechanism of action and the pharmacokinetic properties of vasodilatory drugs facilitates optimal use in clinical practice. It should be kept in mind that a drug belongs to a class but is a distinct entity, sometimes derived from a prototype to achieve a specific effect. The most common pharmacokinetic drug improvement is the development of a drug with a half-life sufficiently long to allow an adequate once-daily dosage. Developing a controlled release preparation can increase the apparent half-life of a drug. Altering the molecular structure may also increase the half-life of a prototype drug. Another desirable improvement is increasing the specificity of a drug, which may result in fewer adverse effects, or more efficacy at the target site. This is especially important for vasodilatory drugs which may be administered over decades for the treatment of hypertension, which usually does not interfere with subjective well-being. Compliance is greatly increased with once-daily dosing. Vasodilatory agents cause relaxation by either a decrease in cytoplasmic calcium, an increase in nitric oxide (NO) or by inhibiting myosin light chain kinase. They are divided into 9 classes: calcium antagonists, potassium channel openers, ACE inhibitors, angiotensin-II receptor antagonists, alpha-adrenergic and imidazole receptor antagonists, beta 1-adrenergic agonist, phosphodiesterase inhibitors, eicosanoids and NO donors. Despite chemical differences, the pharmacokinetic properties of calcium antagonists are similar. Absorption from the gastrointestinal tract is high, with all substances undergoing considerable first-pass metabolism by the liver, resulting in low bioavailability and pronounced individual variation in pharmacokinetics. Renal impairment has little effect on pharmacokinetics since renal elimination of these agents is minimal. Except for the newer drugs of the dihydropyridine type, amlodipine, felodipine, isradipine, nilvadipine, nisoldipine and nitrendipine, the half-life of calcium antagonists is short. Maintaining an effective drug concentration for the remainder of these agents requires multiple daily dosing, in some cases even with controlled release formulations. However, a coat-core preparation of nifedipine has been developed to allow once-daily administration. Adverse effects are directly correlated to the potency of the individual calcium antagonists. Treatment with the potassium channel opener minoxidil is reserved for patients with moderately severe to severe hypertension which is refractory to other treatment. Diazoxide and hydralazine are chiefly used to treat severe hypertensive emergencies, primary pulmonary and malignant hypertension and in severe preeclampsia. ACE inhibitors prevent conversion of angiotensin-I to angiotensin-II and are most effective when renin production is increased. Since ACE is identical to kininase-II, which inactivates the potent endogenous vasodilator bradykinin, ACE inhibition causes a reduction in bradykinin degradation. ACE inhibitors exert cardioprotective and cardioreparative effects by preventing and reversing cardiac fibrosis and ventricular hypertrophy in animal models. The predominant elimination pathway of most ACE inhibitors is via renal excretion. Therefore, renal impairment is associated with reduced elimination and a dosage reduction of 25 to 50% is recommended in patients with moderate to severe renal impairment. Separating angiotensin-II inhibition from bradykinin potentiation has been the goal in developing angiotensin-II receptor antagonists. The incidence of adverse effects of such an agent, losartan, is comparable to that encountered with placebo treatment, and the troublesome cough associated with ACE inhibitors is absent.
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PMID:Clinical pharmacokinetics of vasodilators. Part I. 964 8

A 24 yr old white female presented with dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea, cough and fatigue. Transthoracic echocardiography revealed a sinus venosus atrial septal defect (ASD). Right heart catheterization confirmed severe pulmonary hypertension (80/37 mmHg). A chest radiograph showed enlarged pulmonary arteries with peripheral pruning. Surgical repair of the ASD and lung biopsy were performed. Two days later, she developed right heart failure and was treated with inhaled nitric oxide and then a calcium channel blocker. She failed to improve and was readmitted three months later with severe right heart failure and progressive dyspnoea. While waiting for lung transplantation, she developed haematochezia and died. Light microscopy of lung biopsy and autopsy tissue revealed the structural changes of pulmonary hypertension and focal increases in congested pulmonary capillaries consistent with the diagnosis of pulmonary capillary haemangiomatosis. Quantitative analysis demonstrated that the pathological changes were rapidly progressive.
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PMID:Pulmonary capillary haemangiomatosis coexistence with sinus venosus ASD: morphometric analysis and literature review. 970 45


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