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Titolo:
TIME-COURSE OF CHANGES IN ADENOSINE 5'-MONOPHOSPHATE AIRWAY RESPONSIVENESS WITH INHALED HEPARIN IN ALLERGIC-ASTHMA
Autore:
POLOSA R; MAGRI S; VANCHERI C; ARMATO F; SANTONOCITO G; MISTRETTA A; CRIMI N;
Indirizzi:
UNIV CATANIA,IST MALATTIE APPARATO RESP,VIA PASS GRAVINA 187 I-95125 CATANIA ITALY
Titolo Testata:
Journal of allergy and clinical immunology
fascicolo: 3, volume: 99, anno: 1997,
pagine: 338 - 344
SICI:
0091-6749(1997)99:3<338:TOCIA5>2.0.ZU;2-V
Fonte:
ISI
Lingua:
ENG
Soggetto:
LUNG MAST-CELLS; INOSITOL TRISPHOSPHATE RECEPTOR; VASCULAR SMOOTH-MUSCLE; ANTIGEN-INDUCED AIRWAY; BRONCHOCONSTRICTOR RESPONSE; IPRATROPIUM BROMIDE; HISTAMINE-RELEASE; ORAL TERFENADINE; CALCIUM RELEASE; INHIBITION;
Keywords:
ASTHMA BRONCHOCONSTRICTION; ADENOSINE; HEPARIN;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
45
Recensione:
Indirizzi per estratti:
Citazione:
R. Polosa et al., "TIME-COURSE OF CHANGES IN ADENOSINE 5'-MONOPHOSPHATE AIRWAY RESPONSIVENESS WITH INHALED HEPARIN IN ALLERGIC-ASTHMA", Journal of allergy and clinical immunology, 99(3), 1997, pp. 338-344

Abstract

Background: Recent studies have shown that inhaled heparin exerts a protective effect against various bronchoconstrictor stimuli in asthma,possible through an inhibition of mast cell activation. Objective: Because adenosine 5'-monophosphate (AMP) elicits bronchoconstriction by augmenting mast cell mediator release, we have investigated the effectof inhaled heparin (15,000 units USP/ml, 4 mi) on the bronchoconstrictor response to this agonist and to methacholine in a randomized, double-blind, placebo-controlled study of 10 subjects with asthma. We alsocarried out a separate randomized, double-blind study in seven additional volunteers with asthma to examine in more detail the time-course of change in bronchial reactivity to inhaled AMP after treatment with nebulized heparin. Results: Inhaled heparin significantly increased the provocative concentration of AMP causing a 20% decrease in forced expiratory volume in 1 second (PC(20)FEV(1)-AMP) from the postplacebo treatment value of 22.3 mg/ml (range, 5.7 to 68.9 mg/ml) to 48.1 mg/ml (range, 5.1 196.8 mg/ml) (p < 0.01). When compared with placebo, inhaled heparin failed to alter the airway responsiveness to methacholine; the mean (range) PC20 methacholine values were 1.00 mg/ml (0.44 to 4.76mg/ml) and 1.08 mg/ml (0.46 to 5.08 mg/ml), respectively. After placebo administration, the PC20 AMP values at 15, 60, and 180 minutes did not differ significantly from each other; their geometric mean (range)values were 26.1 mg/ml (5.9 to 85.8 mg/ml), 26.6 mg/ml (6.3 to 87.8 mg/ml), and 24.9 mg/ml (5.2 to 80.2 mg/ml), respectively. When comparedwith placebo, the PC20 values for AMP after administration of inhaledheparin were significantly increased up to 57.3 mg/ml (14.7 to 176.0 mg/ml) and to 52.7 mg/ml (13.9 to 90.8 mg/ml) at 15 minutes and 60 minutes, respectively. At 180 minutes, inhaled heparin failed to affect AMP airway responsiveness; the PC20 AMP was not significantly differentfrom that of placebo, with a value of 30.6 mg/ml (4.8 to 93.3 mg/ml). Conclusion: Heparin administered by inhalation is effective in attenuating the airway response to AMP but not to methacholine. The time course of change in bronchial reactivity to AMP has a peak effect at 15 minutes and lasts up to 60 minutes. It is possible that the mechanism(s) underlying the protective effects of inhaled heparin in asthma may be related to an inhibitory modulation of mast cell activation.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 24/09/20 alle ore 05:24:56