Effect Of Hyperbaric Oxygen On Brain Injury And Memory Deficit In Rats After Acute Carbon Monoxide Poisoning

Acute carbon monoxide (CO) poisoning is one of the common reasons for acute poisoning, and it is one of the main reasons of the death caused by acute poisoning. It's reported that there are 3800 patients died because of acute carbon monoxide poisoning. The number is about one half of that died of acute poisoning. At present, there are not detailed data of morbidity and mortality about acute CO poisoning in out country. But according as all kinds of data, the morbidity of acute CO poisoning is comparative high in our country. From 1992 to 1994, 2842 accidental deathsdue to acute vocationally poisoning are reported in China. Thereinto, there are 1384 accidental deaths due to acute carbon monoxide poisoning. The proportion of carbon monoxide poisoning to acute vocationally poisoning is highest.Since the effect of hyperbaric oxygen (HBO) on acute carbon monoxide was known in 1960s, hyperbaric oxygen has became the mainstay of treatment for acute carbon monoxide poisoning. People have made a lot of research on the mechanism of hyperbaric oxygen. All these research found that Hyperbaric oxygen has many benefits. The half-life of carboxyhaemoglobin at 3 ATA (absolute atmospheres) of oxygen is only 23 minutes. Other benefits are improved mitochondrial function, impairment of platelet adhesion in the capillaries and inhibition of lipid peroxidation. But contrary to expectation, clinical trials of hyperbaric oxygen have given conflicting results. A recent Cochrane review of three major randomized controlled trials concluded that there is as yet no evidence of neurological benefit at one month. Ongoing trials will soon provide further information. In the absence of firm evidence most centres continue using hyperbaric oxygen if the carboxyhaemoglobin is above 25-30%. Myocardial ischaemia and neurological signs, especially coma, are treated with hyperbaric oxygen irrespective of the concentration. All these found and conclusions have explained the effect of hyperbaric oxygen on acute carbon monoxide poisoning. However this research is only in the beginning and there are several questions to be considered firstly: 1) what is the mechanism of delayed neurological syndrome (DNS) induced by acute carbon monoxide poisoning? 2) Whether hyperbaric oxygen treatment has the effect on delayed neurological syndrome induced by acute carbon monoxide poisoning and what is the mechanism of hyperbaric oxygen treatment.-6-Based on these questions, we produced acute carbon monoxide poisoning animal model designed by Ischiropoulos. General hematoxylin-eosin(H&E) stain and immunohistochemistry stain were used to observe the neurological damage in the brain of rat at different time after CO exposure (include 6h> ld> 3d, 5d> 7d, 14d and 21d). Y-maze and Step-Down type passive avoidance task were used to assess the effects of the CO exposure on learning and memory. We compared HBO-treated group with CO-exposed group to assess the effects of hyperbaric oxygen on carbon monoxide poisoning. At the same time to detect neural apoptosis, electron microscopy, immunohistochemistry stain of Bcl-2 and terminal deoxy-nucleotidyl transferase mediated UTP end labeling (TUNEL) were used to assess the effect of HBO on neural apoptosis induced by CO poisoning. The main results of present work are as follows:I) A stable method for the acute CO poisoning animal model: wedescribed the curve of arterial HbCO in the rats which were exposed to CO with different concentration and confirmed feasible exposing concentration and time. Exposed in 2500 parts per million (ppm) carbon monoxide will make the arterial HbCO of rats increased to 65%-70%. All rats loss of conscious (LOG) and the mortality is low (2%).II) Acute oedema and diffuse pathology injury in the brain of rats following acute CO poisoning: Oedema was observed in the brain of rats in the first 3 days after CO exposed. Compared with control group, the brain water content increased significantly (P<0.01). Neural necrosis was observed in cortex, hippocampus, striatum, and cerebellum...