Objective: Direct brain compression and secondary injury due to increased intracranial pressure are believed to be the pathognomic causes of a grave outcome in acute subdural hemorrhage (aSDH). However, ischemic damage from aSDH has received limited attention. The authors hypothesized that cerebral microcirculation is altered after aSDH. Direct visualization of microcirculation was conducted in a novel rat model.
Methods: A craniectomy was performed on each of the 18 experimental adult Wistar rats, followed by superfusion of autologous arterial blood onto the cortical surface. Changes in microcirculation were recorded by capillary videoscopy. Blood flow and the partial pressure of oxygen in the brain tissue (PbtO2) were measured at various depths from the cortex. The brain was then sectioned for pathological examination. The effects of aspirin pretreatment were also examined.
Results: Instantaneous vasospasm of small cortical arteries after aSDH was observed; thrombosis also developed 120 minutes after aSDH. Reductions in blood flow and PbtO2 were found at depths of 2-4 mm. Blood-brain barrier disruption and thrombi formation were confirmed using immunohistochemical staining, while aspirin pretreatment reduced thrombosis and the impairment of microcirculation.
Conclusions: Microcirculation impairment was demonstrated in this aSDH model. Aspirin pretreatment prevented the diffuse thrombosis of cortical and subcortical vessels after aSDH.
Keywords: BBB = blood-brain barrier; CCD = charge-coupled device; GLUT1 = glucose transporter 1; ICH = intracerebral hemorrhage; ICP = intracranial pressure; IHC = immunohistochemical; IP = intraperitoneal; PBS = phosphate-buffered saline; PbtO2 = partial pressure of oxygen in the brain tissue; RBC = red blood cell; SAH = subarachnoid hemorrhage; SMA = smooth muscle actin; SVZ = subventricular zone; TBI = traumatic brain injury; aSDH = acute subdural hemorrhage; acute subdural hemorrhage; aspirin; microcirculation; rat model; trauma.