| Craniocerebral injury, as a kind of severe and complicated trauma, includes not only primary damages in central nervous system due to the external forces, but also secondary damages, which are important reasons for the high mortality and morbidity rates. Many biochemical substances, like acetylcholine, calcium ion, catecholamine, excitatory aminoacids, endogenous opioid peptides, oxygen free radicals, are blamed for the initiation of the secondary damages. These substances are called endogenous brain injury factors, among which calcium ion is the most conspicuous. Calcium ion acts as an important messenger in neurons and it is involved in the syntheses and releases of neurotransmitters, maintenance of excitability of neurons, plasticity of synapses and the activities of many enzymes. It exerts its effects by the changes in intracellular and extracelluar concentrations. In normal rest conditions there exists 10,000 times differences between the concentrations inside and outside cells. When cells are stimulated, extracellular calcium ions flow into cells mainly through voltage-dependent calcium channels (VDCC) and receptor-operated calcium channels (RQCC) so intracellular calcium ion concentration surges, which is very conmon in all kinds of brain injuries, and more severely, calcium overloading in the cytosol occurs. At present it -4- is widely accepted that intracellular calcium overloading determines the initiation and development of secondary damages and it is a final common pathway to cell death. The concrete reasons leading to intracellular calcium overloading are not very clear so far, but it is believed that extracellular calcium ions?inflow in large quantities through calcium channels is the main reason for intracellular calcium overloading. Calcium overloading will trigger a cascade of reactions: (1) to activate phospholipase A2 and increase the production of oxygen free radicals which can hyperoxidize cell memberanes; (2) to activate calmodulin (CaM), which can combine with specific enzymes such as proteinase, endonuclease, leading to the destruction of neuronal skeleton; (3) to combine with mitochondrial memberanes and block the transfer of electrons and ATP production. All these reactions will damage neurons directly or indirectly. The protective effect of mild hypothermia on brain has been widely accepted. In 1991, for the first time, Jiang JY testified that the temperature of 30-33 憕C could protect the animals insulted with brain injury. It could lower the mortality rates of animals; prompt the recovery of motor function; prevent secondary raised JCP; attenuate the pathological impairments of brain tissue. But the exact mechanisms are not very clear. This experiment discusses the metabolic rules of calcium ions under mild hypothermic condition as well as testifies the calcium overloading phenomenon by the measurement of changes in the concentrations of calcium ions after brain injury with laser scanning confocal microscope so as to discover the relationship between calcium ions and mild hypothermia therpy. Materials and Methods -5- Wistar rats of both sexes were subjected to experimental craniocerebral injury induced by a free falling device. 54 rats were divided into 3 groups: (1)...
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