| The degeneration and necrosis of nerve cells are proved to be concerned with anoxia and ischemia after the acute cerebral injury(ACI). ET is recently regarded as the most effective contractile protein in the body for blood vessels and it is also a kind of endogenous injury factor,inducing and aggravating anoxic and ischemic brain injury. Conversely ,CGRP is the most effective substance to expand blood vessels ; meanwhile ,it is an endogenous protective factor,playing an important role in regulating brain vessels and brain blood flow. Both of them contribute to regulate blood vessels of brain and its volume of blood flow. So, the changes of ET and CGRP can accordingly reflect the blood circulation and injury degree of brain tissue. Now hyperbaric oxygenation therapy(HBOT) has been practiced widely in clinical treatment of the acute cerebral injury (ACI).And it has produced a good curative effect .The experimental and clinical studies also demonstrate that HBOT can alleviate brain edema and nerve cells' lesion caused by ACI.Therefore ,HBOT can decrease the fatality rate of ACI and improve the functional recovery of nerve cells .The researches on the mechanism show that HBOT can induce the contractile and expansile reaction of brain vessels, regulate the blood input of brain and impove the blood supply. But very few studies focus on the mechanism study of HBOT's effect on ET and CGRP in the acute cerebral injury.In this experiment, the model of the acute cerebral injury rat is adopted .We measured ET and CGRP concentrations in plasma and injuried cortex by RIA before and after traumatic brain injury during acute stage and also observed the influence of HBO therapy on both of them in order to find the treatment mechanism of HBO for ACI.The results are as follows:1. Compared with the normal group, ET concentration of rats in plasma and injuried cortex are both markedly increased after ACI(p<0.05), and decreased when they come to peak after 24 hours.2. Compared with the normal group, CGRP concentration of rats in plasma and injuried cortex are both decreased after ACI(p<0.05), and at 6h,24h,48h group,they have a rising tendency.3. Compared with the ACI control, ET concentration in plasma and injuried cortex at each time group is decreased after HBO therapy(p<0.05). However, compared with the ACI control, there is no significant change of ET concentration after N2-O2 therapy.4. Compared with the ACI control, CGRP concentration in plasma and injuried cortex at each time group is increased after HBO therapy(p<0.05), among which the concentration of 48h group is higher than that of the normal group. But there is no significant change of CGRP concentration after N2-O2 therapy.5. The change of ET and CGRP at each time group has presented a certain negative corrrelation after traumatic brain injury , HBO therapy and N2-O2 treatment.The above results show:The increase of ET and decrease of CGRP concentration after traumatic brain injury can lead to deterioration of injuried brain tissue, which may be concerned with their regulation by contracting or expanding brain vessels and unbalance of auto-regulation of brain blood flow to reduce the blood volume and oxygen supply of brain tissues. Whereas HBO therapy can decrease ET and increase CGRP, so it can be used as a treatment on brain injury to raise oxygen supply and improve the recovery of injured brain tissue through regulating the brain vessels and correcting the unbalance of auto-regulation of brain blood flow to lesson cerebral edema and neurons injury. |
PDF Full Text Request