TY - JOUR
T1 - Differential effects of ozone on airway and tissue mechanics in obese mice
AU - Rivera-Sanchez, Y. M.
AU - Johnston, R. A.
AU - Schwartzman, I. N.
AU - Valone, J.
AU - Silverman, E. S.
AU - Fredberg, J. J.
AU - Shore, S. A.
PY - 2004/6
Y1 - 2004/6
N2 - Obesity is an important risk factor for asthma. We recently reported increased ozone (O3)-induced hyperresponsiveness to methacholine in obese mice (Shore SA, Rivera-Sanchez YM, Schwartzman IN, and Johnston RA. J Appl Physiol 95: 938-945, 2003). The purpose of this study was to determine whether this increased hyperresponsiveness is the result of changes in the airways, the lung tissue, or both. To that end, we examined the effect of O 3 (2 parts/million for 3 h) on methacholine-induced changes in lung mechanics with the use of a forced oscillation technique in wild-type C57BL/6J mice and mice obese because of a genetic deficiency in leptin (ob/ob mice). In ob/ob mice, 03 increased baseline values for all parameters measured in the study: airway resistance (Raw), lung tissue resistance (Rtis), lung tissue damping (G) and elastance (H), and lung hysteresivity (η). In contrast, no effect of O3 on baseline mechanics was observed in wild-type mice. O3 exposure significantly increased Raw, Rtis, lung resistance (RL), G, H, and η responses to methacholine in both groups of mice. For G, Rtis, and RL there was a significant effect of obesity on the response to O 3. Our results demonstrate that both airways and lung tissue contribute to the hyperresponsiveness that occurs after O3 exposure in wild-type mice. Our results also demonstrate that changes in the lung tissue rather than the airways account for the amplification of O3-induced hyperresponsiveness observed in obese mice.
AB - Obesity is an important risk factor for asthma. We recently reported increased ozone (O3)-induced hyperresponsiveness to methacholine in obese mice (Shore SA, Rivera-Sanchez YM, Schwartzman IN, and Johnston RA. J Appl Physiol 95: 938-945, 2003). The purpose of this study was to determine whether this increased hyperresponsiveness is the result of changes in the airways, the lung tissue, or both. To that end, we examined the effect of O 3 (2 parts/million for 3 h) on methacholine-induced changes in lung mechanics with the use of a forced oscillation technique in wild-type C57BL/6J mice and mice obese because of a genetic deficiency in leptin (ob/ob mice). In ob/ob mice, 03 increased baseline values for all parameters measured in the study: airway resistance (Raw), lung tissue resistance (Rtis), lung tissue damping (G) and elastance (H), and lung hysteresivity (η). In contrast, no effect of O3 on baseline mechanics was observed in wild-type mice. O3 exposure significantly increased Raw, Rtis, lung resistance (RL), G, H, and η responses to methacholine in both groups of mice. For G, Rtis, and RL there was a significant effect of obesity on the response to O 3. Our results demonstrate that both airways and lung tissue contribute to the hyperresponsiveness that occurs after O3 exposure in wild-type mice. Our results also demonstrate that changes in the lung tissue rather than the airways account for the amplification of O3-induced hyperresponsiveness observed in obese mice.
KW - Airway responsiveness
KW - Elastance
KW - Hysterisivity
KW - Leptin
KW - Methacholine
KW - Tissue damping
UR - http://www.scopus.com/inward/record.url?scp=2442657932&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=2442657932&partnerID=8YFLogxK
U2 - 10.1152/japplphysiol.00960.2003
DO - 10.1152/japplphysiol.00960.2003
M3 - Article
C2 - 14966019
AN - SCOPUS:2442657932
SN - 8750-7587
VL - 96
SP - 2200
EP - 2206
JO - Journal of applied physiology
JF - Journal of applied physiology
IS - 6
ER -