Focal brain trauma in the cryogenic lesion model in mice.

Furat Raslan, Christiane Albert-Weißenberger, Ralf-Ingo Ernestus, Christoph Kleinschnitz, Anna-Leena Sirén
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引用次数: 16

Abstract

The method to induce unilateral cryogenic lesions was first described in 1958 by Klatzo. We describe here an adaptation of this model that allows reliable measurement of lesion volume and vasogenic edema by 2, 3, 5-triphenyltetrazolium chloride-staining and Evans blue extravasation in mice. A copper or aluminium cylinder with a tip diameter of 2.5 mm is cooled with liquid nitrogen and placed on the exposed skull bone over the parietal cortex (coordinates from bregma: 1.5 mm posterior, 1.5 mm lateral). The tip diameter and the contact time between the tip and the parietal skull determine the extent of cryolesion. Due to an early damage of the blood brain barrier, the cryogenic cortical injury is characterized by vasogenic edema, marked brain swelling, and inflammation. The lesion grows during the first 24 hours, a process involving complex interactions between endothelial cells, immune cells, cerebral blood flow, and the intracranial pressure. These contribute substantially to the damage from the initial injury. The major advantage of the cryogenic lesion model is the circumscribed and highly reproducible lesion size and location.

Abstract Image

Abstract Image

Abstract Image

小鼠低温损伤模型的局灶性脑损伤。
单侧低温病变的诱导方法由Klatzo于1958年首次提出。我们在此描述了该模型的适应性,该模型允许通过2,3,5 -三苯四唑氯染色和Evans蓝外渗在小鼠中可靠地测量病变体积和血管源性水肿。一个尖端直径为2.5毫米的铜或铝圆柱体用液氮冷却,放置在顶骨皮质上方暴露的颅骨上(坐标来自布雷格玛:后1.5毫米,侧1.5毫米)。尖端的直径和尖端与头盖骨顶接触的时间决定了冻疮的程度。由于血脑屏障的早期损伤,低温皮质损伤的特征是血管源性水肿,明显的脑肿胀和炎症。病变在最初的24小时内生长,这一过程涉及内皮细胞、免疫细胞、脑血流和颅内压之间复杂的相互作用。这些因素在很大程度上促成了最初伤害造成的损害。低温损伤模型的主要优点是损伤的大小和位置是有限制和高度可重复性的。
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