CEREBRAL BLOOD-FLOW AND EDEMA IN PERINATAL HYPOXIC-ISCHEMIC BRAIN-DAMAGE
CEREBRAL BLOOD-FLOW AND EDEMA IN PERINATAL HYPOXIC-ISCHEMIC BRAIN-DAMAGE
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DOI：
10.1203/00006450-199005000-00007
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发表时间：
1990-05-01
影响因子：
3.6
通讯作者：
VANNUCCI, RC
中科院分区：
文献类型：
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作者：
MUJSCE, DJ;CHRISTENSEN, MA;VANNUCCI, RC
在围产期缺氧缺血性脑损伤的实验模型上，研究了脑血流量（CBF）与脑水肿演变的关系。出生后7天的大鼠进行单侧颈总动脉结扎，随后在37 ℃下用8%氧气缺氧3小时。C.在大多数动物中，这种损伤仅在动脉闭塞的同侧大脑半球中产生神经元坏死和/或梗死;单独的缺氧不产生损伤。在脑缺氧缺血恢复期间，以特定的时间间隔同时测定两个大脑半球的CBF（使用碘[14 C]-安替比林通过指示剂扩散技术测量）和组织含水量。在30 min、4 h、24 h、3 d和6 d时，同侧大脑半球的含水量分别为89.1、89.6、89.7、91.0和88.3%（p < 0.001）;而对侧大脑半球的组织含水量百分比与未结扎缺氧对照大鼠的数值（87.7%）相比无变化。在恢复30 min、4 h和24 h时（50-65 mL/100 g/min），两个大脑半球的CBF相似，与年龄匹配的对照组无差异。在第3和6天，同侧大脑半球的CBF分别为对侧大脑半球的30%和26%，对照组动物的23%和29%（P <0.001）。脑含水量的变化与CBF在任何时间段，直到6d的恢复之间不存在负相关。因此，早期低灌注并不遵循围产期脑缺氧缺血，发生在成人。在恢复后15-50小时，发生晚期灌注不足，这是由于组织坏死而不是引起组织坏死。结果表明，通过减少缺氧缺血后脑水肿来改善CBF的治疗尝试不会改变最终的神经病理结果。
The relationship between cerebral blood flow (CBF) and the evolution of brain edema was investigated in an experimental model of perinatal hypoxic-ischemic brain damage. Seven-d postnatal rats were subjected to unilateral common carotid artery ligation followed by 3 h of hypoxia with 8% oxygen at 37.degree. C. This insult produces neuronal necrosis and/or infarction only in the cerebral hemisphere ipsilateral to the arterial occlusion in the majority of animals; hypoxia alone produces no damage. CBF, measured by the indicator diffusion technique using iodo[14C]-antipyrine, and tissue water content were determined concurrently in both cerebral hemispheres at specific intervals during recovery from cerebral hypoxia-ischemia. Water contents in the ipsilateral cerebral hemisphere were 89.1, 89.6, 89.7, 91.0, and 88.3% at 30 min, 4 h, 24 h, 3 d, and 6 d, respectively (p < 0.001); whereas the percent tissue water in the contralateral hemisphere was unchanged from values in nonligated, hypoxic control rats (87.7%). CBF was similar in both cerebral hemispheres at 30 min, 4 h, and 24 of recovery (50-65 mL/100 g/min) and not different from age-matched controls. At 3 and 6 d, CBF in the ipsilateral cerebral hemisphere was 30 and 26% of the contralateral hemisphere and 23 and 29% of the control animals, respectively (P < .0.001). No inverse correlation existed between the changes in brain water content and CBF at any interval until 6 d of recovery. Thus, an early hypoperfusion does not follow perinatal cerebral hypoxia-ischemia, as occurs in adults. A late hypoperfusion takes place that results from rather than causes tissue necrosis seen histologically at 15-50 h of recovery. The results suggest that therapeutic attempts to improve CBF by reducing cerebral edema after hypoxia-ischemia will not alter ultimate neuropathologic outcome.