국소적 뇌손상에 따른 국소 뇌혈류 변화와 뇌부종 형성에 대한 실험적 연구 : An Experimental Gerbil Model = The Effects of Focal Brain Injury on Regional Cerebral Blood Flow and Oedema Formation

다국어 초록 (Multilingual Abstract)

An experimental trauma model in gerbils is described in which we have attempted to produce a focal laceration and contusion. This experimental main objective was to replicate some of the mechanisms involving in human brain injuries, and observe the effect of focal brain injury on regional cerebral blood flow and oedema formation.
80 adult gerbils weighing 40 to 60 gm, were used in this study. The components of the pathophysiological responses, systemic changes, and regional cerebral blood flow (rCBF) associated with the focal brain laceration injury were studied in groups pf animals.
Three groups were studied.
A mild injury (20 animals) was produced by moving the drill along a predetermined pathway through the right orbit at 50 revs per minute over 2 seconds and a severe injury (20 animals) produced in a similar fashion at 200 revs per minute for 8 seconds. An indomethacin preatreated group (20 animals) was produced in a same method of severe injury.
The rCBF measurements were performed immediately after injury in each animal, at 30 minutes and the final few at 60 animal by Pasztor hydrogen clearance technique. Brain specific gravity measurements as an index of brain water was determined in each animal at 1 hour after injury by using Nelson's column gradient method.
There are systemic changes associated with this injury which are neurogenically mediated and results in an immediate reduction to 50 mmHg in blood pressure, a bradycardia and a generalized reduction to 50% -60% in cerebral blood flow during the immediate post-traumatic period. During 30-60 minutes following trauma, a tendency towards slight increasing of blood flow was found in each group, however marked increasing tendency of flow except focal injury site was found in severe injury animal group.
The affects of rCBF are independent of the severity of the local brain injury. These vasomotor effects may induce. Cortical cerebral ischemia and this profoundly influence post-traumatic cerebral function and cause irreversible damage.
There is generalized edema as judged by a decreased brain specific gravity probably related to hypoperfusion secondary to a fall in cardiac output. But there is also superimprosed on this an oedema gradient which is maximal also to the injury. This is turn affects the local capillary flow and further decreases rCBF. In the first hoar after this injury prostaglandins do not appear to be involved in the oedema formation.