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急性实验性脑压迫与减压后脑肿胀的病理生理学

Pathophysiology of brain swelling after acute experimental brain compression and decompression.

作者信息

Xu B N, Yabuki A, Mishina H, Miyazaki M, Maeda M, Ishii S

机构信息

Department of Neurosurgery, Juntendo University, Japan.

出版信息

Neurosurgery. 1993 Feb;32(2):289-96; discussion 296. doi: 10.1227/00006123-199302000-00019.

Abstract

Global ischemia was created by controlled expansion of an epidural balloon for 25 minutes in Group A (six cats) and for 5 minutes in Group B (six cats). The alterations of intracranial pressure, arteriovenous oxygen content difference, cerebral metabolic rate of oxygen, cerebral blood flow, and electroencephalogram were observed until brain death or 24 hours' survival with normal intracranial pressure. The animals were then killed for brain histological examination. In four other cats, a 2% solution of Evans blue dye (4 mg/kg) was injected intravenously--immediately after deflation--resulting in 25 minutes of global ischemia. Two other cats received 5 minutes of global ischemia. The cats were killed 1 hour later. Abrupt swelling occurred in Group A, and no swelling was found in Group B. A transient absolute hyperemia was found immediately after deflation in both groups. The cerebral blood flow and cerebral metabolic rate of oxygen decreased markedly with low arteriovenous oxygen content difference and flat electroencephalogram in Group A, compared with gradual recovery of cerebral blood flow and cerebral metabolic rate of oxygen with high arteriovenous oxygen content difference and reappearance of electroencephalogram activity in Group B. The extravasation of Evans blue was observed on the compressed cerebral hemisphere, thalamus, hypothalamus, and brain stem in swelling animals and only on the compressed hemisphere in nonswelling animals. Histologically, the damage and congestive dilation of capillary, degeneration, and necrosis of neuronal and glial cell were found prominently on the hypothalamus and brain stem in the swelling group.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

在A组(6只猫)中,通过控制硬膜外球囊扩张25分钟来制造全脑缺血,在B组(6只猫)中扩张5分钟。观察颅内压、动静脉氧含量差、脑氧代谢率、脑血流量和脑电图的变化,直至脑死亡或存活24小时且颅内压正常。然后处死动物进行脑组织学检查。在另外4只猫中,放气后立即静脉注射2%伊文思蓝染料溶液(4毫克/千克),造成25分钟的全脑缺血。另外2只猫经历5分钟的全脑缺血。1小时后处死这些猫。A组出现突然肿胀,B组未发现肿胀。两组在放气后立即出现短暂的绝对充血。与B组脑血流量和脑氧代谢率逐渐恢复、动静脉氧含量差高且脑电图活动重新出现相比,A组脑血流量和脑氧代谢率显著降低,动静脉氧含量差低且脑电图平坦。在肿胀动物的受压脑半球、丘脑、下丘脑和脑干观察到伊文思蓝外渗,在未肿胀动物中仅在受压半球观察到。组织学上,肿胀组下丘脑和脑干的毛细血管损伤和充血性扩张、神经元和神经胶质细胞变性和坏死明显。(摘要截短于250字)

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