CEREBROSPINAL-FLUID PRESSURE CHANGES AFTER ACUTE CARBON-MONOXIDE POISONING AND THERAPEUTIC EFFECTS OF NORMOBARIC AND HYPERBARIC-OXYGEN IN CONSCIOUS RATS

This study on conscious rats with occluded left carotid artery investi gates the influence of cerebral edema after acute carbon monoxide (GO) poisoning on cerebrospinal fluid pressure (CSFp) and evaluates the th erapeutic effectiveness of normobaric oxygen (NBO2) and hyperbaric oxy gen (HBO2). The CSFp was continuously recorded via a cannula placed in the left cerebral ventricle before, during, and for up to 6 h after e xposure to 0.27% CO for 1 h. A non-sustained small increase in the CSF p and identical degrees of hypoxemia, hypocapnia, arterial hypotension , and acidosis were found during the exposure in all rats. After the C O exposure, all non-edema control rats without carotid artery ligation (n = 7) recovered completely with normal CSFp, behavior, and brain wa ter content. All untreated (n = 7) and NBO2-treated rats (n = 7) devel oped a severely increased CSFp (>50 mmHg) with neurologic motor dysfun ction, and died of a severely increased CSFp (>100 mmHg) with consider able cerebellar herniation. Except in one rat, the CSFp did not reach a dangerous level (>25 mmHg) after the HBO2 session (300 kPa O-2 for 1 h, beginning at 20 min post-CO). All HBO2-treated rats (n = 7) surviv ed with less neurologic motor dysfunction and less left hemispheric ed ema than those in untreated and NBO2-treated rats. The results demonst rated that the increase in the CSFp was related to the left hemispheri c edema, and that the cerebellar herniation was the predominant cause of death after the CO exposure. HBO2, but not NBO2, prevented the seve re increase in the CSFp and thus saved the life after the CO exposure.