Stavert D M, Lehnert B E
Life Sciences Division, Los Alamos National Laboratory, New Mexico 87545.
Environ Res. 1989 Feb;48(1):87-99. doi: 10.1016/s0013-9351(89)80088-x.
Previous investigations have indicated that postexposure exercise (E) can can potentiate nitrogen dioxide (NO2)-induced lung injury. In this report, we (1) further characterize the potentiation of expression of NO2-induced lung injury in the rat by E; (2) characterize the postexposure period during which such potentiation by E can occur, i.e., "window of susceptibility"; (3) assess whether two E bouts performed during the "window of susceptibility" have even greater potentiating effects; and (4) determine if early postexposure E can extend the window of susceptibility. Groups of Fischer-344 rats were exposed to 100 ppm NO2 for 15 min, exercised at times ranging from 30 min to 24 hr thereafter, and sacrificed during a 24-hr postexposure period. Other exposed rats were exercised 30 min to 24 hr thereafter and sacrificed for lung studies 30 min following the E runs. Still other exposed animals were exercised immediately and at 8 or 24 hr postexposure and sacrificed 30 min after the last E run. NO2-exposed but rested rats, and sham-air-exposed and rested or exercised rats served as controls. E immediately or at 8 hr post-NO2 exposure caused marked increases in lung wet weight (LWW) and right cranial lobe dry weights (RCLDW) and more pronounced histopathologic disturbances beyond those following NO2 exposure and rest only. Potentiation of injury was not observed in rats exercised 24 hr after exposure. The pattern of subsidence of the LWW and RCLDW increases after immediate or 8 hr E differed with the increases in the former being more persistent. Two E bouts (30 min and 8 hr postexposure) caused lung changes consistent with an additive effect. E performed immediately after NO2 exposure extended the window of susceptibility to E beyond 24 hr.