Viability Of Cells Essay Example

nervous system. Study detected that the neuronal damage occurred due to over activation of glutamate receptors. After SCI, Excitatory amino acids, glutamate and aspirates are peak up within few minutes. In the spinal cord, the concentration of extracellular excitatory amino acid arrived to the toxic level within 15 minutes till 120 minutes. However, extracellular excitatory amino acids have much toxic effect for the neurons during the SCI.

Apoptosis is found after SCI in human being which is accelerated due to the release of cytokines, inflammation, free radicals as well as excitotoxicity. After 3 hours to 8 weeks in traumatic SCI, the death of apoptotic cell is seen.

From the experimental studies, after a few week of injury occurring of dimyelinization was intensified by apoptosis in oligodentrocytes. Crow et.al showed that oligodentrocytic changes in SCI for the initial period. Furthermore, apoptosis adversely affects the result due to the increasing neuronal loss. From some studies it is proved that apoptosis deteriorates in microglia to secondary inflammatory injury. From the experimental studies showed that the activation of caspase overstated by SCI. Signals activating apoptosis trigger caspases and can play active role in the three pathways of apoptosis. The death of apoptotic cell causes in all cellular components including neurons, astrocytes, oligodentrocytes also microglia. Neuronal protection is most important as there is no capability to reproduce neurons in the spinal cord. Though glias can regenerate potential and inhibit the glial death support of neuronal protection by two similar pathways. Initially, neurotrophic and metabolic support are provided by glia to injured neurons which is essential for the supporting of recovery. Finally, apoptotic mediators including cytokines, free radicals leak out from dying cells

which have toxicity to adjacent cells.

From a study proved that opioid peptides are locally released in spinal cord injuries. Endogenous opioids which have significantly role to the mechanism of secondary injury due to blockage of opiate receptors. A study also showed that by administration of non-selective antagonist for example naloxone after acute SCI, spinal cord blood flows and clinical status of patient were improved.

The concentration of electrolytes changed after spinal cord trauma which was showed from the experimental studies. Chronic SCI which is increased axonal message with 4-aminopyridine and a recovery sign showed in mild levels. From cats model with SCI, it was also proved about the similar effect of 4-aminopyridinine by blocking the fast K+ channels. Formation glutamate and free radicals are significantly increased by the cause of lipid perfusion injury. Antagonism of glutamate in endothelium can prevent the devastation of blood spinal cord barrier. It has been proved that neurological results are improved by glutamate receptor blockers in SCI. Magnesium ions can decrease the lipid per-oxidation process by the antagonism of glutamate receptors. Calcium ions also can play role in death cells. Calcium ions those can promote the cell damage by the activation of phospholipases, proteases and phosphorylases in the cells. Another experimental study proved that calcium channel blockers can significantly prevent the secondary SCI. Many experimental studies are proving that blood flowing to the spinal cord is being improved by those agents also has significantly positive activity on healing. Study has been demonstrated that blood flowing and neurological recoveries are promoted by dopamine, adrenaline, nimodipine and dextran after SCI.

Decreasing blood supply of substantial is caused by severe SCI and ischemia initiated after

the trauma. Blood flowing to the spinal card which’s otoregulation was disrupted incarnates changes of systemic hemodynamic. That’s why the ischemia produced by SCI may be collapsed due to systemic hypotention and hypoxia. The transportation of glucose and oxygen to the tissue can be collapsed down due to the ischemia and decrease ATP generation. The exact cause of post-traumatic ischemia is not clearly learnt. However, Focal narrowing of sulcal arterioles and in-tramedullary capillaries, fragmentation, aneurysmal dilatation or occlusion have been developed which found in experimental studies. A study demonstrated with the help of Evans blue technique, progressive vascular damage in spinal cord contusion injury model for the first time. In that study the uptake of Evans blue increased about 76% in the injury area 24th hour likened to those second hour. PH of tissue may be increased because of lactic acidosis. Because of the accumulation of fibrin and platelets, congestion and venous stasis are caused. Moreover, ischemia may be occurred by the damaging of capillary endothelium, edema, petechial hemorrhages and vasoactive cytokines. For this, the systems are resulted to anaerobic respiration. Many pathophysiological processes can be caused by ischemia and activation of anaerobic respiration. Edema may be caused in the site of injury and peripheral tissues by the proteinaceous leakage via intrinsic spinal cord veins. Spinal cord pressure can be increased by edema and the disruption of blood flow of the spinal card occurred. A study has been showed that magnesium can reduce edema also vascular permeability in SCI.