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Effect of high dose inhaled acetic acid on airway responsiveness in Fischer rats: DISCUSSION (1)

RESULTS

Immediate postexposure response: RL and EL increased significantly in the study group (n=11). Apart from a transient, postexposure increase in RL and EL, we did not demonstrate a significant change in lung mechanics or airway responsiveness, measured 24 h and one week after the insult. This occurred despite exposure to a concentrated (8 N = 50%) acetic acid solution administered in a manner identical to that of the Mch aerosol. It is, therefore, difficult to assume that irritant delivery to the lower airways failed. It can be argued that studying a larger number of animals would possibly reveal ‘irritant susceptible individuals’. However, inbred animal species tend to be uniform in their airway response, as shown in our study (Tables 1,2; Figures 3,4). Furthermore, individual ‘asthma-like susceptibility’ cannot be consistently demonstrated in animal models. The relative hyper-responsiveness of the Fischer rat strain is probably explained by structural characteristics of parenchymal-airway interdependence. A single study in guinea-pigs demonstrating AHR14 days after intratracheal instillation of sulphur mustard (a chemical warfare agent) was found in the literature. Transient AHR (measured 90 mins postexposure) was also demonstrated in guinea-pigs exposed to acid-coated, ultrafine fly ash particles. AHR could not be demonstrated with exposure to either sulphur dioxide or the particles alone. One study in Sprague-Dawley rats reported changes in Mch responsiveness after chlorine gas exposure. Other animal studies failed to show AHR, even following recurrent exposures. Thus, the agents that have induced AHR in animal models have not been those generally described in human studies. buy ortho tri-cyclen online

Figure 3. Effect of high dose inhaled acetic
Figure 3) a Postexposure lung resistance (RL). b Postexposure lung elasticity (EL). Control animals (n=3, open square; mean ± SE), study group data (n=11), and individual (lines) and group means ±SE (solid squares) are shown. Both RL (180% of baseline) and EL (167% of baseline) increased transiently at 1 min postexposure compared with baseline, 5 min and control animal values (P<0.001)

Table 1. Lung resistance (Rl) and lung elastance (El) after exposure to acetic acid

0 1 Time (min) 5 15 30
RL, mean ± SD (cm H2O/mL/s)
Study (n=11) 0.256±0.043 0.460±0.062* 0.286±0.054 0.247±0.035 0.253±0.039
Control (n=3) 0.243±0.036 0.261±0.049 0.245±0.037 0.243±0.040 0.251±0.032
EL, mean ± SD (cm H2O/mL)
Study (n=11) 3.278±0.493 5.476±0.695* 3.041±0.433 3.299±0.472 3.334±0.442
Control (n=3) 2.973±0.440 2.720±0.050 3.505±0.226 3.249±0.652 3.423±0.734

*P < 0.02 versus all other time periods in the same animal and P

Table 2. Lung resistance (RL), lung elastance (EL) and the concentration of methylcholine require to double Rl (ED200RL) at baseline, one day and one week postexposure

Baseline Day1 7
RL, mean±SD
(cm H2O/mL/s)
Study (n=11) 0.219±0.055 0.251±0.042 0.260±0.067
Control (n=3) 0.225±0.063 0.259±0.043 0.235±0.055
EL mean±SD
(cm H2O/mL)
Study (n=11) 6.304±1.595 6.206±1.293 5.770±1.122
Control (n=3) 5.939±0.857 5.745±0.897 6.815±0.598
ED200RL
(geometric mean)
Study (n=11) 7.142 7.959 6.784
Control (n=3) 8.009 6.486 7.777

Values did not change significantly at one and seven days postexposure. Values were similar between control and study animals

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