Umezawa H, Shima K, Chigasaki H, Sato K, Ishii S
Department of Neurosurgery, National Defence Medical College Saitama, Japan.
Acta Neurochir Suppl (Wien). 1990;51:351-3. doi: 10.1007/978-3-7091-9115-6_119.
Two hydrostatic factors such as acute hypertension and decompressive craniectomy were chosen and assessment was focused on how the hydrostatic pressure gradient altered the cerebrovascular dynamics and metabolism during the process of development of brain oedema. Hydrostatic oedema was induced by bolus injection of autologous blood through the common carotid artery in Sprague-Dawley rats. Rats were divided into two groups, one with craniectomy (Cr+) and the other without craniectomy (Cr-). Animals were sacrificed immediately, 24 and 48 h after the hypertensive insult. Brain water content was determined by the gravimetric method. Regional cerebral blood flow (rCBF) and glucose metabolism (1CGU) were measured by quantitative autoradiographic methods using 14C-iodoantipyrine and 14C-deoxyglucose, respectively. The hypertensive insult produced multifocal lesions stained by Evans blue. In the brains of the Cr- group, there was a transient increase in water content and no significant change of rCBF and 1CGU. In the Cr+ group, the increase in water content was pronounced and continued until 48 h later. In addition, misery perfusion was observed at 24 h after the insult and both rCBF and 1CGU were significantly decreased after 48 h. These results indicate that the increased hydrostatic pressure gradient enhances tissue damage and causes the reopening of blood-brain barrier.
选取了急性高血压和减压颅骨切除术这两个流体静力因素，并重点评估在脑水肿发展过程中流体静水压梯度如何改变脑血管动力学和代谢。通过经颈总动脉推注自体血在Sprague-Dawley大鼠中诱导流体静力性水肿。将大鼠分为两组，一组进行颅骨切除术（Cr+），另一组不进行颅骨切除术（Cr-）。在高血压损伤后立即、24小时和48小时处死动物。采用重量法测定脑含水量。分别使用14C-碘安替比林和14C-脱氧葡萄糖通过定量放射自显影法测量局部脑血流量（rCBF）和葡萄糖代谢（1CGU）。高血压损伤产生了伊文思蓝染色的多灶性病变。在Cr-组的大脑中，含水量短暂增加，rCBF和1CGU无显著变化。在Cr+组中，含水量增加明显并持续至48小时后。此外，在损伤后24小时观察到灌注不良，48小时后rCBF和1CGU均显著降低。这些结果表明，增加的流体静水压梯度会加重组织损伤并导致血脑屏障重新开放。
