Lack of late-phase airway responses in conscious guinea pigs after a variety of antigen challenges

1992 ◽  
Vol 37 (3-4) ◽  
pp. 191-194 ◽  
Author(s):  
D. C. Underwood ◽  
R. R. Osborn ◽  
J. M. Hand
1991 ◽  
Vol 199 (3) ◽  
pp. 271-278 ◽  
Author(s):  
Takehisa Iwama ◽  
Ken-ichi Shikada ◽  
Akiko Yamamoto ◽  
Mitsuaki Sakashita ◽  
Morihide Hibi ◽  
...  

1992 ◽  
Vol 73 (5) ◽  
pp. 1847-1853 ◽  
Author(s):  
S. A. Shore ◽  
M. A. Martins ◽  
J. M. Drazen

We examined the effects of the selective neutral endopeptidase (NEP) inhibitor SCH32615 on airway responses to rapid intravenous infusions of substance P (SP) and neurokinin A (NKA) and on recovery of administered tachykinins from arterial blood in anesthetized mechanically ventilated guinea pigs. SCH32615, in doses that cause a marked increase in the magnitude of bronchoconstriction induced by infused NKA, had little effect on the changes in pulmonary conductance (GL) or dynamic compliance induced by SP. In animals in which SCH32615 (1 mg/kg) was administered in combination with the angiotensin-converting enzyme (ACE) inhibitor captopril (5.7 mg/kg), the dose of SP required to decrease GL by 50% was fourfold less than in animals that received captopril alone (P < 0.005). SP measured in arterial blood withdrawn within 45 s of intravenous administration of this tachykinin was not different in control and SCH32615-treated animals, whereas captopril caused an approximately threefold increase in SP concentrations (P < 0.005). When SCH32615 and captopril were administered together, significantly more SP was recovered than when captopril or SCH32615 was administered alone (P < 0.0005). Our results are consistent with the hypothesis that both NEP and ACE contribute to the degradation of intravenously infused SP. ACE degradation of SP is sufficient to limit SP-induced bronchoconstriction even in the presence of specific NEP inhibition.


1992 ◽  
Vol 37 (3-4) ◽  
pp. 178-180 ◽  
Author(s):  
I. M. Richards ◽  
R. L. Griffin ◽  
S. K. Shields ◽  
M. S. Reid ◽  
S. F. Fidler
Keyword(s):  

1986 ◽  
Vol 60 (6) ◽  
pp. 2089-2093 ◽  
Author(s):  
K. P. Agrawal ◽  
R. E. Hyatt

Tracheal Na+-K+-ATPase activity is positively correlated with in vivo airway responsiveness to histamine. We wondered whether this were a chance association or whether it was directly related to the mechanism of hyperreactivity. Therefore, we obtained dose-response curves to aerosols of histamine and ouabain in guinea pigs to determine whether an in vivo relationship existed between the excitatory effects of histamine and the enzyme-inhibiting effect of ouabain. Airway responsiveness to ouabain was measured as the ouabain concentration producing a 30% decrease in specific airway conductance (ED30) or that producing a half-maximal response (ED50). Responsiveness to histamine was measured either as ED30 or as ED50. Significant positive correlations were noted between the log ED50 of ouabain and log histamine ED30 or ED50 (r = 0.81 and 0.83, respectively; P less than 0.001), and between log ouabain ED30 and log histamine ED30 and ED50 (r = 0.76 and 0.77, respectively; P less than 0.002). Pretreatment with ouabain increased airway responsiveness to histamine (P less than 0.05). We suggest that in hyperreactive airways Na+-K+-ATPase serves a homeostatic function of preventing Na+ and Ca2+ loading of the cell and that it is not directly responsible for the hyperreactivity.


1991 ◽  
Vol 94 (1-4) ◽  
pp. 293-294 ◽  
Author(s):  
R.W. Gristwood ◽  
J. Llupiá ◽  
A.G. Fernández ◽  
P. Berga

1997 ◽  
Vol 156 (3) ◽  
pp. 696-703 ◽  
Author(s):  
WILLIAM M. ABRAHAM ◽  
ASHFAQ AHMED ◽  
MAREK W. SIELCZAK ◽  
MASAHIRO NARITA ◽  
THOMAS ARRHENIUS ◽  
...  

2000 ◽  
Vol 403 (3) ◽  
pp. 267-275 ◽  
Author(s):  
Hiroyuki Nakano ◽  
Hisamichi Aizawa ◽  
Koichiro Matsumoto ◽  
Satoru Fukuyama ◽  
Hiromasa Inoue ◽  
...  

1997 ◽  
Vol 328 (1) ◽  
pp. 75-81 ◽  
Author(s):  
Kozaburo Ikegami ◽  
Hiroko Hata ◽  
Jun-ichi Fuchigami ◽  
Katsuyuki Tanaka ◽  
Yoshiro Kohjimoto ◽  
...  

1989 ◽  
Vol 67 (5) ◽  
pp. 1764-1769 ◽  
Author(s):  
C. Clerici ◽  
I. Macquin-Mavier ◽  
A. Harf

The contribution of the nonadrenergic inhibitory system to airway responses to infusion of 5-hydroxytryptamine (5-HT) was evaluated in anesthetized, tracheotomized, and paralyzed young (13 days) and adult (82 days) guinea pigs. Animals were mechanically ventilated by a constant flow ventilator. Compliance (C) and conductance (G) of the respiratory system were continuously monitored. Three series of experiments were performed involving intravenous pretreatment with 1) atropine (3 mg/kg) and propranolol (1 mg/kg); 2) atropine (3 mg/kg), propranolol (1 mg/kg), and phentolamine (2 mg/kg); and 3) atropine (3 mg/kg) and hexamethonium (2 mg/kg). 5-HT was then intravenously infused for 5 min at a rate of 40 ng.kg-1.s-1 in adults and 60 ng.kg-1.s-1 in young guinea pigs to obtain the same degree of bronchoconstriction in both groups. At the 3rd min of the infusion, bilateral cervical vagotomy was performed and C and G were measured at the maximal response, 1-2 min thereafter. Vagotomy increased bronchoconstriction (P less than 0.01) in both young animals and adults. Phentolamine did not modify this increase, but hexamethonium completely inhibited it. These results indicate that, in adult and young guinea pigs, 5-HT infusion induces reflex activation of the nonadrenergic inhibitory system, which in turn modulates the bronchoconstrictor responses to 5-HT. This neural modulation is not mediated by an alpha-adrenergic pathway.


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