Inhaled ammonium persulphate inhibits non-adrenergic, non-cholinergic relaxations in the guinea pig isolated trachea.
BACKGROUND
Persulphates can act both as irritants and sensitizers in inducing occupational asthma. A dysfunction of nervous control regulating the airway tone has been hypothesized as a mechanism underlying bronchoconstriction in asthma.


OBJECTIVE
It was the aim of this study to investigate whether inhaled ammonium persulphate affects the non-adrenergic, non-cholinergic (NANC) inhibitory innervation, the cholinergic nerve-mediated contraction or the muscular response to the spasmogens, carbachol or histamine, in the guinea pig epithelium-free, isolated trachea.


METHODS
Male guinea pigs inhaled aerosols containing ammonium persulphate (10 mg/m(3) for 30 min for 5 days during 3 weeks). Control animals inhaled saline aerosol. NANC relaxations to electrical field stimulation at 3 Hz were evaluated in whole tracheal segments as intraluminal pressure changes. Drugs inactivating peptide transmission, nitric oxide synthase, carbon monoxide production by haem oxygenase-2 and soluble guanylyl cyclase were used to assess the involvement of various inhibitory neurotransmitters. Carbachol and histamine cumulative concentration-response curves were obtained.


RESULTS
In both groups, nitric oxide and carbon monoxide participated to the same extent as inhibitory neurotransmitters. In exposed animals, the tracheal NANC relaxations were reduced to 45.9 +/- 12.1% (p < 0.01). The cholinergic nerve-mediated contractions to electrical field stimulation and the muscular response to histamine were not modified by ammonium persulphate exposure. The muscular response to carbachol was unaffected up to 1 microM. Conversely, the response to the maximal concentration of carbachol (3 microM) was increased (p < 0.01).


CONCLUSIONS
Ammonium persulphate inhalation at high concentrations impairs the nervous NANC inhibitory control in the guinea pig airways. This may represent a novel mechanism contributing to persulphate-induced asthma.
Dellabianca
A
A
Department of Preventive, Occupational and Community Medicine, University of Pavia, Pavia, Italy. antonio.dellabianca @ unipv.it
Faniglione
M
M
De Angelis
S
S
Colucci
M
M
Cervio
M
M
Balestra
B
B
Tonini
S
S
Candura
S M
SM
D000280:Administration, Inhalation; D000645:Ammonium Sulfate / Q000494:pharmacology*; D000818:Animals; D002217:Carbachol / Q000494:pharmacology; D002248:Carbon Monoxide / Q000502:physiology; D002452:Cell Count; D018679:Cholinergic Agonists / Q000494:pharmacology; D004558:Electric Stimulation; D004804:Eosinophils / Q000473:pathology; D006168:Guinea Pigs; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects / Q000502:physiology; D009126:Muscle Relaxation / Q000187:drug effects* / Q000502:physiology; D009130:Muscle, Smooth / Q000187:drug effects / Q000294:innervation / Q000502:physiology; D009504:Neutrophils / Q000473:pathology; D009569:Nitric Oxide / Q000502:physiology; D014132:Trachea / Q000294:innervation* / Q000473:pathology / Q000502:physiology; D014660:Vasoactive Intestinal Peptide / Q000502:physiology
D018679:Cholinergic Agonists; C031276:ammonium peroxydisulfate; D009569:Nitric Oxide; D014660:Vasoactive Intestinal Peptide; D002248:Carbon Monoxide; D002217:Carbachol; D000645:Ammonium Sulfate