Abstract
The effects of heparin were studied concurrently with development of neurological and respiratory signs of oxygen toxicity in awake unrestrained rats exposed to 3 atmosphere absolute (ATA) oxygen. The modification of the early electrophysiological manifestations of CNS oxygen toxicity by heparin in the absence of obvious signs of pulmonary oxygen toxicity was also determined at 5 ATA oxygen by electrocorticographic recording. The femoral artery of all rats was cannulated two days before the exposures to hyperbaric oxygenation (HBO), and the effect of intraarterial injection of 10 U/100g/3h heparin or an equivalent volume of saline was studied in experimental and control rats, respectively. In rats exposed to 3 ATA oxygen, the latency of the onset of the first oxygen-induced convulsions, the time interval between the first convulsion and death, and the survival time were measured. Exposure to 5 ATA oxygen was continued until the onset of the first preconvulsive paroxysmal electrical discharges (FED), considered to be an early electrophysiological indicator of CNS oxygen toxicity. The onset of convulsions was slightly delayed in heparin-treated rats exposed to 3 ATA oxygen, and the time interval between the first convulsions and death was significantly reduced in heparinized rats. No difference in survival time between heparin- and saline-treated rats was observed. Heparin significantly delayed the time of onset of the FED during exposure to 5 ATA oxygen. Gross postmortem examination of the lungs and internal organs revealed only a bloody froth in the trachea of the heparin- treated rats exposed to 3 ATA oxygen. It is concluded that the heparin-hyperoxic interaction during development of pulmonary and CNS oxygen toxicity may be related to the anticoagulant effect of heparin and hyperoxic-induced pulmonary lesions.
Published Version
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