Arito H, Takahashi M, Sotoyama M, Tsuruta H, Ishikawa T
National Institute of Industrial Health, Kawasaki, Japan.
Arch Toxicol. 1993;67(3):193-9. doi: 10.1007/BF01973307.
Effects of trichloroethylene (TRI) on the central nervous system (CNS) and autonomic functions were examined by means of continuous polygraphic measurements of electroencephalogram (EEG), electromyogram (EMG) and electrocardiogram (ECG) in electrode-implanted and freely moving rats, while they were exposed via inhalation to TRI vapor of 300, 1000 or 3000 ppm for 8 h/day or 6000 ppm for 4 h/day on 3 consecutive days. The exposures to 3000 and 6000 ppm produced abnormal EEG activity and incapacitation of postural maintenance during the exposure period, while the post-exposure period was characterized by decreased waking (W) time, lowered heart rate (HR) and increased numbers of bradyarrhythmic episodes after recovery from anesthesia. The exposure to 1000 ppm decreased W time without the appearance of anesthesia. The exposure to 300 ppm did not produce any observable effects except the lowered HR, which occurred during the post-exposure period. The relationships between internal doses of TRI and its metabolites and these TRI-induced pathophysiological responses were determined by blood and brain analyses of TRI, trichloroethanol and trichloroacetic acid in the TRI-exposed rats. Recordings of respiratory chest wall movement revealed that the number of TRI-induced bradyarrythmias accompanying apnea during paradoxical sleep (PS) increased significantly after cessation of exposure to 6000 ppm TRI. This suggests that TRI-induced hypoxemia due to apnea during PS triggers bradyarrhythmogenesis through increased cardiac vagal efferent tone.
