Shima K, Marmarou A
Richard Roland Reynolds Neurosurgical Research Laboratories, Medical College of Virginia, Richmond 23298.
Adv Neurol. 1990;52:285-7.
We found that under conditions of sustained edema production, the rate of edema resolution by the CSF is not appreciably enhanced with lowering of the ICP. Although the entrance of edema fluid into CSF for the high-pressure series was notably slower, the amount of edema remaining in the brain was not appreciably affected. This appears somewhat contradictory to the principle that increasing the bulk flow pressure gradient should increase flow into the CSF. However, simultaneous steady-state measurements of the change in brain tissue pressure for a corresponding change in CSF pressure showed that the two pressures are identical. As a result, when ICP is lowered, the brain tissue pressure follows with no gradient increase. This also suggests that lowering of ICP and the concomitant reduction of tissue pressure may increase the intravascular tissue pressure gradient, which may act to increase the edema production. More work is required to resolve this issue.
我们发现,在持续产生水肿的情况下,随着颅内压降低,脑脊液消除水肿的速率并未明显提高。尽管高压组中水肿液进入脑脊液的速度明显较慢,但脑中残留的水肿量并未受到明显影响。这似乎与增加体积流压力梯度应增加流入脑脊液的流量这一原则有些矛盾。然而,对脑脊液压力相应变化时脑组织压力变化的同时稳态测量表明,这两种压力是相同的。因此,当颅内压降低时,脑组织压力随之降低,压力梯度并未增加。这也表明,颅内压降低以及随之而来的组织压力降低可能会增加血管内组织压力梯度,这可能会促使水肿产生。需要更多的研究来解决这个问题。