Effects of Increased Intracranial Pressure Gradient on Cerebral Venous Infarction in Rabbits

Abstract

Cerebral venous infarction (CVI) is a rare vascular disease most commonly caused by cerebral venous thrombosis that leads to hemorrhage or infarct formation. A rabbit model of CVI was established by placing a recoverable epidural sacculus to research effects of increased pressure on CVI. Rabbits were randomly divided into the following groups: A, CVI; B, 0.2-mL epidural sacculus placed on the basis of CVI; C, 0.4-mL epidural sacculus; D, 0.6-mL epidural sacculus; E, sham operation. Two sacculus-release groups were then added, 8 hours (group F) and 24 hours (group G), on the basis of group D. Brain water content, extent of cerebral infarction, hemorheology indexes, D dimer, and fibrinogen were observed at 8, 24, and 48 hours after surgery. Brain water content was higher in groups A-D compared with group E with the exception of the 24-hour A group. Brain water content was significantly lower in sacculus-release groups compared with the 48-hour D group. Extent of cerebral infarction in group D was significantly higher at 24 and 48 hours compared with groups A and E. Extent of cerebral infarction in sacculus-release groups was significantly lower compared with group D at 48 hours. Hemorheology indexes and fibrinogen were significantly higher in group D compared with groups A and E at corresponding time points and increased with increasing intracranial pressure. In the rabbit model of CVI, degree of brain edema, extent of cerebral infarction, hemorheology indexes, and fibrinogen increased as intracranial pressure gradient increased, which may promote formation of a hypercoagulable state. Early removal of intracranial hypertension reduced degree of edema and extent of cerebral infarction in rabbits.