The Prevention Of Procyanidins On Oxygen-Induced Convulsion In Mice And Its Mechanism

When people inhale pure oxygen in excess of 200 kPa (2 ATA), they may suffer from acute oxygen toxicity. With main manifestations as generalized, tonic-clonic seizures, acute oxygen toxicity is also defined as central nervous system (CNS) oxygen toxicity or oxygen-induced convulsion. In recent years, the chances of breathing oxygen at higher pressures are more in such activities as military and professional diving, clinical treatment for more and more sicknesses. Because of the poor tolerance to hyperbaric oxygen (HBO), or the fault of device and operation, CNS oxygen toxicity may occur in these courses. So it is imperative to prevent this disease. Although the prevention with medicines is an effective supplementary mean, it is disappointed that satisfying drug has not been found by now, partly for the unnoticeable preventive effects or the adverse effects to the body, especially when administered for long period.We studied the prevention of procyanidins on oxygen-induced convulsion in mice, and proposed that the effect is related with it's antioxygenic property and protection for cerebral vessels in terms of the mechanisms of oxygen toxicity. In the experiments, we studied the convulsion latency, the time of continuous convulsion (TCC) and the convalescence stage after being exposed to HBO of mice injected with procyanidins intraperitoneally, and detected the contents of ROS, MDA, SOD, which are related with oxygen-antioxygen system, and GABA, the most important inhibitory transmitter, synthetic emzyme for GABA in vitro.The results show that the convulsion latency of mice injected with procyanidins intraperitoneally under the pressure of 5 ATA O2 was prolonged prominently and their mortality was reduced, at the same time, the content of ROS and MDA in the cortex and hippocampus was reduced while that of SOD, GABA in these regions was...