C pneumoniae impairs arterial endothelial function, and the NO pathway is principally involved. Cyclooxygenase-dependent vasoconstricting products may also account for the infection-induced impaired relaxation. These findings further support the role of C pneumoniae infection in atherosclerosis development.

SummaryT he objective of the study was to exam ine the changes in central nervous system (CNS) activity and physical behaviour during induction and awakening from CO 2 anaesthesia. Two studies, each using pigs immersed into 90% CO 2 gas for a period of 60 s were performed. In study 1, we monitored middle latency auditory evoked potentials (changes in latencies, amplitudes and a depth of anaesthesia index), electroencephalographic parameters (delta, theta, alpha and beta electroencephalographic power and 95% spectral edge frequency) and heart rate; and in study 2, we monitored body movements and arterial and venous partial pressure of CO 2 and O 2 . No behavioural signs of distress were observed during the early part of the induction. T he swine exhibited muscular activity from 13±30 s after induction-start as well as during awak ening from anaesthesia, possibly because of a transitory weaker suppression of the brain stem than of the cortex. T he CNS and blood gas param eters started to change from the very start of induction. T he CNS suppression lasted only approxim ately one minute after the end of the induction period. T he two studies indicated a good tem poral relationship between changes in amplitude, depth of anaesthesia index, spectral edge frequency, and arterial P CO 2 during the induction period.

The study is part of a series of investigations performed with the ultimate goal of obtaining an objective evaluation of the ethical aspects and the narcotic efficiency of CO2 inhalation used as pre-slaughter anaesthesia for swine. Six Yorkshire swine were exposed twice to 80% CO2 for 1 min during simultaneous recording of the EEGs from the frontal neocortex, the dorsal hippocampus, and the amygdaloid region via permanently implanted electrodes. In five of the animals myoclonic jerks started at 28 +/- 1 s of CO2 exposure and lasted for 6 +/- 2 s. Neocortical slow wave (delta) activity and increased amplitude of the hippocampal theta (5-7 Hz) waves (i.e. EEG changes seen during the second stage of barbiturate anaesthesia) had developed before the brief period of myoclonic jerks. After this period the EEG activity gradually declined, resulting in neocortical EEG silence at the end of the exposure. This apparent isoelectricity lasted for on average 1 min. The return of the neocortical EEG activity exhibited a pattern reverse to its disappearance, but was much prolonged in comparison to the EEG extinction. Pre-exposure neocortical EEG pattern was not regained until 3-5 min post-exposure. In eight out of 11 experiments the CO2 inhalation also induced hippocampal EEG silence lasting for on average 30 s. EEG flattening was further obtained when recording from the amygdaloid nuclear complex and the adjacent pyriform cortex. The observed changes in the neocortical and hippocampal EEGs suggest that the present swine were unconscious already when they exhibited motor reactions. This does not exclude the possibility that CO2-independent stress/arousal factors present in a slaughterhouse environment may facilitate the development of motor phenomena similar to seizures, with the result that such reactions become manifest before the neocortical EEG exhibits an anaesthesia pattern. The duration of the observed EEG silence implies that, from the ethical point of view, exsanguination might safely be performed within 1 min after the moment when the animal is removed from the high concentration CO2. However, the slow return to a pre-exposure neocortical EEG pattern suggests that the swine remains unconscious for at least another minute.