Abstract
AimCarbon monoxide (CO) poisoning can cause permanent damage in tissues that are sensitive to hypoxia. We explored the feasibility and efficacy of using a hyperoxygenated solution (HOS) to treat severe acute CO poisoning in an animal model.MethodsMale Sprague-Dawley rats were subjected to CO poisoning. The HOS was administered into the femoral vein of these rats through a catheter (10 ml/kg). Carboxyhemoglobin (COHb) and blood gases were used to assess the early damage caused by CO poisoning. S100β was measured to predict the development of late cognitive sequelae of CO. The Morris water maze test was performed to assess cognitive function, and Nissl staining was performed to observe histologic change. ResultsThe COHb concentrations rapidly decreased at 5 min after the HOS administration; however, the PaO2 and SaO2 in rats treated with HOS increased significantly 5 min after the HOS administration. The S100β concentrations, which increased significantly after CO poisoning, increased at a much slower rate in the rats treated with HOS (HOS group) compared with the rats treated with O2 inhalation (O2 group). The escape latency in the place navigation test was shortened after CO poisoning on days 11-15 and days 26-30, and the swimming time in quadrant 4 in the spatial probe test on days 15 and 30 after CO poisoning was prolonged in the rats treated with HOS injection compared with the rats treated with oxygen inhalation or normal saline injection. The neuronal degeneration in the HOS group was alleviated than that in the CO or O2 group.ConclusionHOS efficiently alleviates the brain damage in acute CO-poisoned rats and thus may serve as a new way to treat human patients with CO poisoning in clinical practice.
Highlights
Acute carbon monoxide (CO) poisoning continues to be a serious health problem in China and many other countries
We found that the injection of an hyperoxygenated solution (HOS) into rats with acute CO poisoning significantly delayed or attenuated the increases in the COHb and S100β concentrations and the decreases in the PaO2 and SaO2 levels
The decreasing rate of the COHb concentration is affected by the half-life of COHb, which has been reported to be shortened to 40-80 min and 240-320 min by the treatments with 100% oxygen and room air (21% oxygen), respectively [19]
Summary
Acute carbon monoxide (CO) poisoning continues to be a serious health problem in China and many other countries. Despite the aggressive treatment approaches taken in many industrialized countries, the morbidity and mortality rates from CO poisoning have remained high [2]. Half of those who experience CO poisoning have cognitive sequelae between 3 days and 4 weeks after the event, some survivors with severe CO exposure do remain asymptomatic [3,4,5]. Hyperbaric oxygen therapy, which uses pure oxygen to speed and enhance the body’s natural ability to heal, has been broadly used as a medical treatment for CO poisoning [6]. For many patients with CO poisoning, hyperbaric oxygen therapy is contraindicated [7,8,9]. Untreated pneumothorax is an absolute contraindication for hyperbaric oxygen therapy.
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