Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0016382 (flushing)
 6,387 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vasoactive intestinal peptide (VIP) caused significant bronchodilatation in seven asthmatic volunteers when given intravenously at the rate of 6 pmol/kg/min for 15 min during a double-blind study. Tachycardia and cutaneous flushing were observed during the infusion. VIP also ameliorated histamine-induced bronchoconstriction in all subjects. VIP may be an important natural bronchodilator in man and this has implications for the pharmacotherapy of asthma.
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PMID:Vasoactive intestinal peptide causes bronchodilatation and protects against histamine-induced bronchoconstriction in asthmatic subjects. 613 72

Vasoactive intestinal peptide (V.I.P.) caused bronchodilatation in 7 asthmatic volunteers when given intravenously at the rate of 6 pmol kg-1 min-1 for 15 minutes during a double blind study. Mean baseline FEV1 was 2.8 (+/- 0.3 S.E.) which was 81% of predicted and increased by 0.21 (range 0.1-0.45) l after 15 minutes infusion (p greater than 0.02). Tachycardia and cutaneous flushing were also observed during the infusion. Subsequent induced bronchoconstriction with a predetermined dose of histamine was ameliorated at 180 seconds following challenge when compared with placebo. Mean fall in FEV1 0.26 compared with 0.741 when pre-infusion FEV1 was taken on baseline. Mean fall in FEV1 0.49 l compared with 0.75 l when the FEV1 immediately preceding challenge was used on baseline (p greater than 0.02). The demonstration that V.I.P. is a bronchodilator in asthmatics and ameliorates histamine induced bronchoconstriction has important implications for the pharmacology of asthma.
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PMID:Vasoactive intestinal peptide as a bronchodilator in asthmatic subjects. 638 97

Nine patients with mid-gut carcinoid tumours received leucocyte interferon (IFN) i.m. daily for 90 days. Six patients clearly ameliorated in symptoms typical of the carcinoid syndrome (flushing, diarrhoea, asthma) which correlated with reduced serum levels of tumour related polypeptides and urinary output of 5-hydroxyindole acetic acid (5-HIAA). Before IFN treatment, peripheral blood mononuclear leucocytes (PBLs) from carcinoid patients showed markedly deficient production of pH 2 labile IFN-alpha in response to Staphylococcus aureus Cowan I (SACoI) in vitro. In contrast, IFN-alpha responses to the inducers Sendai virus and beta-haemolytic streptococcus group G and IFN-gamma responses to Lens culinaris lectin and concanavalin A were normal. Also, basal and in vitro IFN enhanced natural killer (NK) cell activity and T cell mitogen-induced cell proliferation were similar in patients and controls. During 90 days of IFN therapy, SACoI-induced IFN responses became entirely undetectable. There were transient declines at 1 and 30 days in IFN responses to the other IFN inducers, of mitogen-induced lymphocyte proliferation and of basal NK activities. The increments of NK cell activities after in vitro IFN exposure were clearly decreased in IFN treated patients, suggesting in vivo activation of these cells. Thus, the results demonstrate one remarkable abnormality in carcinoid patients: a deficient IFN response to SACoI and a clear influence of IFN therapy on several parameters of the IFN-NK system.
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PMID:Evaluation of the natural killer cell-interferon system in patients with mid-gut carcinoid tumours treated with leucocyte interferon. 661 63

We compared the effects of inhaled glycopyrrolate (G), 1.3 mg, and atropine (A), 2.6 mg, and placebo on FEV1 and specific conductance (sGaw) before and after exercise in six men with exercise-induced asthma. Subjects exercised with cold air (-2 degrees C) 30 and 120 minutes after each aerosol treatment. Spirometry was performed and sGaw determined before aerosol treatment (baseline) and before and after exercise. Decreased airway tone was noted before exercising with A and G but not with placebo. The decreases in FEV1 and sGaw resulting from exercise were not significantly different among the three treatment groups at either exercise session. Postexercise FEV1 and sGaw were significantly higher after A and G compared to P. Dry mouth, flushing, and resting tachycardia were prominent with group A. Symptoms in G did not differ from those in P. This study suggests that A and G do not prevent bronchoconstriction induced by exercise and cold air but improve postexercise pulmonary function by achieving preexercise bronchodilation. Systemic side effects were minimal with G compared to A.
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PMID:Effect of inhaled glycopyrrolate and atropine in asthma. Precipitated by exercise and cold air inhalation. 669 86

A 39-year-old nurse exhibited for one year an immediate-type asthmatic reaction with rhinorrhea and facial flushing and itching after ingestion of alcohol. The elimination of all alcohol-containing items from the operating theater brought relief from the daytime symptoms. Some dyspnea after salicylate ingestion and in cold weather persisted. Oral provocation tests with wine and pure ethanol and inhalation tests with ethanol vapours gave rise to all the known symptoms. Asthma could be prevented by prior inhalation of disodium cromoglycate, whereas facial itching and nasal reaction was prevented by oral ketotifen but not by cromoglycate.
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PMID:[Asthma and rhinitis induced by the ingestion of pure ethanol and by the inhalation of alcohol vapors]. 680 72

A 23-year-old Asian with histamine-reactive asthma complained of recurrent chest tightness, nasal congestion and flushing immediately after drinking minimal amounts of alcoholic beverages. He was extensively studied to determine the possible mechanism of his alcohol-induced respiratory symptoms. Drinking of either beer or 95 percent ethanol in apple juice immediately provoked vasomotor signs and moderately severe bronchospasm (54 percent and 73 percent decreases in specific airway conductance, respectively), which spontaneously improved over 30 minutes and two hours, respectively. Intravenous and inhaled ethanol caused less bronchospasm than observed with oral ethanol, and recovery was rapid. Pretreatment with cromolyn sodium (inhaled or oral) and isoproterenol had no inhibitory effect on the alcohol-induced bronchoconstriction, whereas atropine, acetylsalicylic acid, cyproheptadine, and chlorpheniramine appeared to have a partial inhibitory effect. Approximately 70 percent inhibition was observed after chlorpheniramine. Observations in this patient suggest that the bronchoconstriction induced by alcoholic beverages is related to their ethanol content and may be related to formation or release of one or more bronchoconstrictor and vasoactive compounds, including a stimulant of histamine1-receptors. The route of ethanol administration may also influence the bronchospastic response.
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PMID:Alcohol-induced bronchospasm in an asthmatic patient: pharmacologic evaluation of the mechanism. 724 61

A total of 291 diabetics were studied to see whether an asthmatic reaction was associated with facial flushing induced by chlorpropamide and alcohol. Of these patients, 191 reported facial flushing, of whom 12 reported breathlessness as well. Of these 12, five also described wheezing, and respiratory function tests showed them to have asthma. Three of these five patients underwent further tests, which showed that the asthmatic reaction could be prevented by giving disodium cromoglycate and the specific opiate antagonist naloxone. One patient developed wheezing when given an enkephalin analogue with opiate-like activity. Asthma induced by chlorpropamide and alcohol was concluded to be mediated by endogenous peptides with opiate-like activity such as enkephalin.
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PMID:Asthma induced by enkephalin. 735 55

Inhaled platelet-activating factor (PAF) provokes considerable pulmonary gas exchange disturbances in normal man and in patients with mild asthma, similar to those observed in acute severe asthma. To further examine the mechanisms involved in PAF-induced ventilation-perfusion (VA/Q) mismatch, eight healthy, non-atopic, nonsmoking subjects were studied after administration of PAF aerosol (24 micrograms). They had been previously treated with inhaled salbutamol (300 micrograms) in a randomized, double-blind, cross-over, placebo-controlled design. After placebo, PAF provoked a fall in total arterial white cell count with a rebound leukocytosis. As shown in a previous study, an overall index of VA/Q inequality (DISP R-E*, 1.64 +/- 0.10) showed a threefold increase (P < 0.006) that accounted for the increase (79%) in AaPO2 (p < 0.04) after PAF, while the respiratory system resistance (Rrs) rose by 16% (p < 0.02). In contrast, after pretreatment with salbutamol inhaled PAF had no effects on pulmonary gas exchange, Rrs, or white cell count; facial flushing and cough were also hindered. The results are consistent with the hypothesis that salbutamol inhibits PAF-induced venoconstriction in both the airway and pulmonary microcirculation.
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PMID:Salbutamol inhibits pulmonary effects of platelet activating factor in man. 776 15

A 54-year-old woman was admitted to our hospital because of an asthmatic attack. Her first asthma attack occurred when she was 53 years old. It was followed by a flu-like infection, and was preceded for one year perennial rhinitis and loss of the sense of smell. Symptoms were perennial, and unrelated to the seasons. Because these clinical findings resembled those of aspirin-induced asthma (AIA), an aspirin-DL-lysine i.v. challenge test was done. Cough, perspiration, and flushing was provoked within 15 min after aspirin-DL-lysine injection, but FEV1 did not change. Respiratory sounds were normal and no wheezing was audible. Other cyclooxygenase inhibitors (ketoprofen, sulpyrine and acetaminophen) provoked the same symptoms. Successively increasing doses of injected aspirin-DL-lysine resulted in complete tolerance to this stimulus. We propose that aspirin-induced cough without bronchoconstriction is a new type of aspirin hypersensitivity.
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PMID:[A case of aspirin-induced cough without bronchoconstriction. A new type of aspirin hypersensitivity]. 779 60

Effect of cetirizine, a potent and specific H1 receptor antagonist, was examined on platelet activating factor-induced bronchoconstriction in 10 patients (5 male, mean [s.e.m.] aged 37.4 [3.6] years) with mild asthma in a placebo controlled, double-blind cross-over study. Airway responses were assessed by measuring specific airway conductance (SGaw). Patients were challenged with a single dose (12-96 micrograms) of PAF that had previously produced a 35% fall in SGaw. PAF challenges were performed after single dose (15 mg) and 1 week's treatment (15 mg twice daily) of cetirizine. There was no significant difference in pre- and post-treatment baseline values of SGaw on different study days and the percentage changes after cetirizine were 38.7 (7.01) and 45.6 (5.52) compared to 50.2 (2.89) and 43.9 (7.26) with placebo respectively. Similarly mean (s.e.m.) area under curve (AUC-SGaw/time course response) was 391 (143) and 514 (85) with cetirizine compared to 565 (37) and 461 (94) with placebo respectively. The difference was not statistically significant. There was no difference in facial flushing and feeling of warmth between cetirizine and placebo. We conclude that PAF induced bronchoconstriction in humans is not mediated by histamine release and that H1 receptor antagonists do not modify PAF induced bronchoconstriction.
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PMID:Effect of cetirizine, a potent H1 antagonist, on platelet activating factor induced bronchoconstriction in asthma. 810 3


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