IB4, a monoclonal antibody against the CD18 leukocyte adhesion protein, reduces intracranial pressure following thromboembolic stroke in the rabbit.
IB4, a monoclonal antibody against the CD18 leukocyte adhesion protein, reduces intracranial pressure following thromboembolic stroke in the rabbit.
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IB4 是一种针对 CD18 白细胞粘附蛋白的单克隆抗体，可降低兔子血栓栓塞性中风后的颅内压。
DOI：
10.1080/01616412.1996.11740398
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发表时间：
1996
影响因子：
1.9
通讯作者：
Gross,CE
中科院分区：
文献类型：
--
作者：
Bednar,MM;Wright,SD;Raymond-Russell,SJ;Kohut,JJ;Gross,CE
脑缺血-再灌注引起的神经元活化和积聚已被认为会加重组织损伤。本研究旨在检测IB 4（一种针对中性粒细胞粘附蛋白CD 18的单克隆抗体）在兔血栓栓塞性卒中模型中的作用。给予新西兰兔（3- 3.5kg，每组n = 8）自体凝块栓塞，通过颈内动脉递送至脑的前循环。血栓栓塞后，立即在所有动物的平均动脉压降低到30毫米汞柱，通过控制放血的时间为45分钟。所有的动物进行机械通气，并监测以下参数每小时：动脉血气，颅内压，局部脑血流量，红细胞压积，和核心温度。在血栓栓塞事件后30分钟给予兔IB 4（1 mg kg-1）或溶媒（1%白蛋白，IV）。在4小时实验的剩余时间内，所有动物的平均动脉压恢复至基线值50-60 mmHg。血栓栓塞事件后，两组的颅内压均升高，但IB 4治疗组的颅内压显著降低，最终值为195.9±38.3 vs. 135.5 =基线的B 26.0%（平均值± SEM，p < 0.05）。然而，两组的局部脑血流量和梗死面积（TTC染色）几乎相同。它的结论是，封锁的中性粒细胞粘附蛋白，CD 18，可能有助于降低颅内压脑缺血和再灌注后，提供进一步的证据表明，激活的中性粒细胞可能有助于脑水肿。[Neurol Res 1996;18：171-175]
Neutrophil activation and accumulation as a consequence of cerebral ischemia-reperfusion has been suggested to exacerbate tissue injury. The current study is designed to examine the effect of IB4, a monoclonal antibody directed against the neutrophil adhesion protein, CD18, in a rabbit model of thromboembolic stroke. New Zealand rabbits (3-3.5 kg n = 8 each group), were given an autologous clot embolus, delivered to the anterior circulation of the brain via the internal carotid artery. Immediately following thromboembolism, the mean arterial pressure in all animals was reduced to 30 mmHg by controlled exsanguination for a period of 45 min. All animals were mechanically ventilated and following parameters were monitored hourly: arterial blood gases, intracranial pressure, regional cerebral blood flow, hematocrit, and core temperature. Rabbits were given either IB4 (1 mg kg-1), or vehicle (1% albumin, IV) 30 min following the thromboembolic event. The mean arterial pressure of all animals was restored to the baseline value of 50-60 mmHg for the remainder of the 4-h experiment. Following the thromboembolic event, the intracranial pressure rose in both groups, although this was significantly less in the IB4-treated group, with the final values being 195.9±38.3 vs. 135.5 =b 26.0% of baseline (mean ± SEM, p < 0.05). However, regional cerebral blood flow and infarct size (TTC staining) were virtually identical in both groups. It is concluded that blockade of the neutrophil adhesion protein, CD18, may contribute to a reduction in the intracranial pressure following cerebral ischemia and reperfusion, providing further evidence that activated neutrophils may contribute to cerebral edema. [Neurol Res 1996;18: 171–175]