TY  - JOUR
A1  - Raslan, Furat
A1  - Albert-Weißenberger, Christiane
A1  - Westermaier, Thomas
A1  - Saker, Saker
A1  - Kleinschmitz, Christoph
A1  - Lee, Jin-Yul
T1  - A modified double injection model of cisterna magna for the study of delayed cerebral vasospasm following subarachnoid hemorrhage in rats
N2  - Delayed cerebral vasospasm following subarachnoid hemorrhage (SAH) is a serious medical complication, characterized by constriction of cerebral arteries leading to varying degrees of cerebral ischemia. Numerous clinical and experimental studies have been performed in the last decades; however, the pathophysiologic mechanism of cerebral vasospasm after SAH still remains unclear. Among a variety of experimental SAH models, the double hemorrhage rat model involving direct injection of autologous arterial blood into the cisterna magna has been used most frequently for the study of delayed cerebral vasospasm following SAH in last years. Despite the simplicity of the technique, the second blood injection into the cisterna magna may result in brainstem injury leading to high mortality. Therefore, a modified double hemorrhage model of cisterna magna has been developed in rat recently. We describe here step by step the surgical technique to induce double SAH and compare the degree of vasospasm with other cisterna magna rat models using histological assessment of the diameter and cross-sectional area of the basilar artery
KW  - Medizin
KW  - Cerebral vasospasm
KW  - Cisterna magna
KW  - Double hemorrhage model
KW  - Rat
KW  - Subarachnoid
Y1  - 2012
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-76038
ER  - 
TY  - JOUR
A1  - Raslan, Furat
A1  - Albert-Weißenberger, Christiane
A1  - Ernestus, Ralf-Ingo
A1  - Kleinschnitz, Christoph
A1  - Sirén, Anna-Leena
T1  - Focal brain trauma in the cryogenic lesion model in mice
N2  - 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.
KW  - Medizin
KW  - Experimental brain trauma
KW  - Cryolesion
KW  - Secondary traumatic brain damage
KW  - Mice
Y1  - 2012
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-75419
ER  - 
TY  - JOUR
A1  - Albert-Weißenberger, Christiane
A1  - Várrallyay, Csanád
A1  - Raslan, Furat
A1  - Kleinschnitz, Christoph
A1  - Sirén, Anna-Leena
T1  - An experimental protocol for mimicking pathomechanisms of traumatic brain injury in mice
N2  - Traumatic brain injury (TBI) is a result of an outside force causing immediate mechanical disruption of brain tissue and delayed pathogenic events. In order to examine injury processes associated with TBI, a number of rodent models to induce brain trauma have been described. However, none of these models covers the entire spectrum of events that might occur in TBI. Here we provide a thorough methodological description of a straightforward closed head weight drop mouse model to assess brain injuries close to the clinical conditions of human TBI.
KW  - Medizin
KW  - closed head injury
KW  - traumatic brain injury
KW  - neurobehavioural deficits
KW  - astrocyte
KW  - microglia
KW  - neurons
Y1  - 2012
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-75368
ER  -