| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1997: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1996: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1995: ¥800,000 (Direct Cost: ¥800,000)
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| Research Abstract |
Cerebral contusious sometimes cause progressive or delayd deterioration of neurological symptoms, which may result from secondary injury processes of the traumatized brain. It is important to elucidate pathophysiology underlying secondary brain damages, since one principal goal of treatments for traumatic brain injury is to prevent such secondary damages following the injury. In the present syudy, in order to elucidate the mechanisms of contusion-induced secondary cell injury processes, we investigated hemodynamic changes in cerebral contusion, and effects of anti-thrombosis and anti-coagulate drugs were tested in a rat cortical contusion induced by a controlled cortical impact device. Results (1)Histological examinations revealed that the initial histopathological finding in the peripheral area of contusion was microthrombosis formation, followed by brain edema and necrosis formation. These changes progressively extended to peripheral area surrounding the contusion. (2)In the central
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area of contusion, cerebral blood flow (CBF) was decreased to the ischemic level within 5-15 min after the injury induction. In the peripheral area, CBF was decreased to 20% of the beseline, returned to 40-60% level, and then decreased again to the ischemic level without any recovery. (3)A inhibitor of platelet activating factor (PAF), etizolam, attenuated the contusional necrosis formation as well as decreasing CBF in the peripheral but not in the central area of contusion. (4)The tissue osmolality of contusion increased immediately following the injury, and the tissue water content increased thereafter. (5)The concentration of the tissue cations (total amount of [Na^+]+[K^+] in the contusion did not show any significant changes, indicating inorganic ions do not mainly participate in the tissue osmolality increase. Discussion The results of the present study indicate that the microthrombosis formation in the peripheral areas of contusion may contribute to the secondary cell injury processes in cerebral contusion. Anti-thrombosis with a PAF antagonist has a therapeutic potential to attenuate the lschemic btain damage and subsequent edema formation following the contusion. The progressive increase in tissue osmolality is another cause of contusion-induced edema formation. Increases in metabolic intermediate osmoles and/or idiogenic osmoles resulting from the catabolic degradation of intracellular high molecular substances, e.g.phospholipids in cell membrane, may play a major role for the formation of osmotic potential and a resultant brain edema in the cerebral contusion. Less
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