Maximal Forced Expiratory Maneuver to Measure Airway Obstruction in Anesthetized Guinea Pigs

Respiration ◽  
1997 ◽  
Vol 64 (4) ◽  
pp. 257-262 ◽  
Author(s):  
Ching-Chi Lin ◽  
Ching-Yuang Lin
2001 ◽  
Vol 91 (3) ◽  
pp. 1061-1066 ◽  
Author(s):  
Timothy D. Mickleborough ◽  
Robert W. Gotshall ◽  
Jann Rhodes ◽  
Alan Tucker ◽  
Loren Cordain

Previous studies have indicated that increased dietary salt consumption worsens postexercise pulmonary function in humans with exercise-induced asthma (EIA). It has been suggested that EIA and hyperpnea-induced airway obstruction (HIAO) in guinea pigs (an animal model of EIA) are mediated by similar mechanisms. Therefore, the purpose of this study was to determine whether altering dietary salt consumption also exacerbated HIAO in guinea pigs. Furthermore, the potential pathway of action of dietary salt was investigated by blocking leukotriene (LT) production during HIAO in guinea pigs. Thirty-two male Hartley strain guinea pigs were split into two groups. One group ( n = 16) of animals ingested a normal-salt diet (NSD) for 2 wk; the other group ( n = 16) ingested a high-salt diet (HSD) for 2 wk. Thereafter, animals were anesthetized, cannulated, tracheotomized, and mechanically ventilated during a baseline period and during two dry gas hyperpnea challenges. After the first challenge, the animals were administered either saline or nordihydroguaiaretic acid, a LT inhibitor. Bladder urine was analyzed for electrolyte concentrations and urinary LTE4. The HSD elicited higher airway inspiratory pressures (Ptr) than the NSD ( P < 0.001) postchallenge. However, after infusion of the LT inhibitor and a second hyperpnea challenge, HIAO was blocked in both diet groups ( P < 0.001). Nonetheless, the HSD group continued to demonstrate slightly higher Ptr than the NSD group ( P < 0.05). Urinary LTE4 excretion significantly increased in the HSD group compared with the NSD group within treatment groups. This study has demonstrated that dietary salt loading exacerbated the development of HIAO in guinea pigs and that LT release was involved in HIAO and may be moderated by changes in dietary salt loading.


1992 ◽  
Vol 72 (2) ◽  
pp. 434-438 ◽  
Author(s):  
J. A. Karlsson ◽  
N. B. Choudry ◽  
C. Zackrisson ◽  
R. W. Fuller

The effects of nebulized diuretics on citric acid-induced cough and airway obstruction in guinea pigs and capsaicin-induced cough and increase in airway resistance in humans have been studied. Half-maximum inhibition of cough in the guinea pig was produced by 1.3 mM furosemide and 0.25 mM hydrochlorothiazide. Cough was inhibited by 78 +/- 9% by 3 mM furosemide (P less than 0.05) and 89 +/- 11% by 3 mM hydrochlorothiazide (P less than 0.01). At the same time, airway obstruction was inhibited by 50 +/- 9% (P less than 0.001) and 42 +/- 15% (P less than 0.05), respectively. Nebulized furosemide (3 mM) was without effect on the airway obstruction produced by inhaled histamine or acetylcholine in the guinea pigs. Intravenously administered furosemide (270 nmol/kg) did not affect citric acid-induced responses. In humans, aerosolized furosemide (9 mM) and hydrochlorothiazide (3.4 mM) reduced the percent increase in respiratory resistance from 22.1 +/- 3.7 and 15.6 +/- 3.4 to 10.5 +/- 4.9 and 9.4 +/- 3.3%, respectively (P less than 0.05), but were without effect on cough due to capsaicin. Thus both furosemide and hydrochlorothiazide inhibited airway obstruction in the guinea pig and reduced the capsaicin-induced increase in airway resistance in humans. However, whereas coughing was inhibited in the guinea pig, neither drug affected cough in humans. This difference in the action of the loop diuretic and thiazide, which interact differently with Na(+)-K(+)-Cl-transport within the airway mucosa, on the cough and airflow obstruction in guinea pig and humans supports the view that different sensory limbs are involved in these reflexes.(ABSTRACT TRUNCATED AT 250 WORDS)


2001 ◽  
Vol 33 (5) ◽  
pp. S58
Author(s):  
T D. Mickleborough ◽  
R W. Gotshall ◽  
J Rhodes ◽  
A Tucker ◽  
L Cordain

2002 ◽  
Vol 130 (1) ◽  
pp. 79-87 ◽  
Author(s):  
Ching-Chi Lin ◽  
Ching-Fen Chang ◽  
Shwu-Fang Liaw ◽  
Ching-Yuang Lin

2013 ◽  
Vol 125 (10) ◽  
pp. 471-482 ◽  
Author(s):  
William R. Ford ◽  
Alan E. Blair ◽  
Rhys L. Evans ◽  
Elinor John ◽  
Joachim J. Bugert ◽  
...  

Viral exacerbations of allergen-induced pulmonary inflammation in pre-clinical models reportedly reduce the efficacy of glucocorticoids to limit pulmonary inflammation and airways hyper-responsiveness to inhaled spasmogens. However, exacerbations of airway obstruction induced by allergen challenge have not yet been studied. hPIV-3 (human parainfluenza type 3 virus) inoculation of guinea-pigs increased inflammatory cell counts in BAL (bronchoalveolar lavage) fluid and caused hyper-responsiveness to inhaled histamine. Both responses were abolished by treatment with either dexamethasone (20 mg/kg of body weight, subcutaneous, once a day) or fluticasone propionate (a 0.5 mg/ml solution aerosolized and inhaled over 15 min, twice a day). In ovalbumin-sensitized guinea-pigs, allergen (ovalbumin) challenge caused two phases of airway obstruction [measured as changes in sGaw (specific airways conductance) using whole body plethysmography]: an immediate phase lasting between 4 and 6 h and a late phase at about 7 h. The late phase, airway hyper-responsiveness to histamine and inflammatory cell counts in BAL were all significantly reduced by either glucocorticoid. Inoculation of guinea-pigs sensitized to ovalbumin with hPIV-3 transformed the allergen-induced airway obstruction from two transient phases into a single sustained response lasting up to 12 h. This exacerbated airway obstruction and airway hyper-responsiveness to histamine were unaffected by treatment with either glucocorticoid whereas inflammatory cell counts in BAL were only partially inhibited. Virus- or allergen-induced pulmonary inflammation, individually, are glucocorticoid-sensitive, but in combination generate a phenotype where glucocorticoid efficacy is impaired. This suggests that during respiratory virus infection, glucocorticoids might be less effective in limiting pulmonary inflammation associated with asthma.


2007 ◽  
Vol 557 (1) ◽  
pp. 66-68 ◽  
Author(s):  
Peter W. Stengel ◽  
Sandra L. Cockerham ◽  
Steven A. Silbaugh

1995 ◽  
Vol 79 (6) ◽  
pp. 2148-2153 ◽  
Author(s):  
P. W. Stengel ◽  
C. A. Yiamouyiannis ◽  
R. L. Obenchain ◽  
S. L. Cockerham ◽  
S. A. Silbaugh

Postmortem pulmonary gas trapping was investigated as an index of in vivo airway obstruction following methacholine inhalation in four different rodent species. Male guinea pigs (Hartley), hamsters (golden Syrian), mice (A/J, BALB/c, and ICR), and rats (Brown-Norway, Fischer 344, Lewis, and Sprague-Dawley) were exposed to aerosols of methacholine or sodium chloride. Maximum excised lung gas volumes (ELGV) of methacholine-exposed guinea pigs, hamsters, mice, and rats were 2.3–8.7 times those of sodium chloride-treated animals. Mean ELGV values of sodium chloride-exposed animals ranged from 1.50 +/- 0.20 ml/kg for guinea pigs to 2.75 +/- 0.20 ml/kg for Brown-Norway rats. Although all species responded to methacholine, guinea pigs were the most responsive, with approximately 1.6 microgram/kg of inhaled methacholine needed to increase ELGV to 200% of control. Compared with guinea pigs, hamsters, mice, and rats were 11- to 1,395-fold less responsive. Although hamsters, mice, and rats are less sensitive than guinea pigs to the airway-obstructive effects of methacholine, pulmonary gas trapping appears useful as a measure of airway responses in these species.


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