LATERAL CORTICAL IMPACT INJURY IN RATS - CEREBROVASCULAR EFFECTS OF VARYING DEPTH OF CORTICAL DEFORMATION AND IMPACT VELOCITY

Intracranial pressure (ICP), blood pressure (BP), cerebral perfusion p ressure (CPP), and cortical perfusion (LDF) of the contralateral parie tal cortex were measured after cortical impact injury in 36 rats. Chan ges in these physiologic parameters were compared using analysis of va riance to a group of 11 rats who received a sham impact. In one series of experiments, the velocity and duration of the impact injury were k ept constant, and the severity of the injury was determined by varying the depth of cortical deformation from 2 to 3 mm. The peak pressure i nside the skull was directly related to the depth of cortical deformat ion, and was 93 +/- 16, 182 +/- 18, and 268 +/- 57 mm Hg with the 2, 2 .5, and 3 mm deformation, respectively, when the impact velocity was 5 m/sec. With the 2 mm depth injury, there was a transient decrease in BP (p < 0.05) and a 12% decrease in LDF after the impact. With the 2.5 mm depth injury, a small transient increase in ICP and decrease in BP and a 30% decrease in LDF occurred (p < 0.05). ICP then gradually inc reased throughout the 8 h experiment, becoming significantly greater t han the sham-injured animals by 5 h after the impact. LDF gradually re turned toward normal throughout the experiment. With the 3 mm depth in jury, a marked transient increase in ICP (p < 0.05) and BP (p < 0.05) occurred immediately after the impact. The increase in BP lasted <5 mi n, and subsequently the BP decreased to approximately 50 mm Hg for the rest of the experiment. The initial marked increase in ICP lasted 15 min and then remained 5-10 mm Hg higher (p < 0.05) than in the sham-in jured animals for the rest of the experiment. LDF decreased by an aver age of 50% (p < 0.05) immediately after the impact and remained lower than that of the sham-injured animals for the rest of the experiment. In another series of experiments, the depth of cortical deformation wa s kept constant at 2.5 mm, and the severity of the injury was determin ed by varying the velocity from 1 to 5 m/sec. The peak ICP was signifi cantly related to the impact velocity, averaging 45 +/- 12, 66 +/- 9, and 182 +/- 18 mm Hg with the 1, 3, and 5 m/sec impact injuries, respe ctively. The 1 m/sec impact had no effect on ICP and only a transient decrease in BP. LDF was initially slightly decreased but, beginning at 4 h after the impact, increased to levels greater than for the sham-i njured animals (p < 0.05). The 3 m/sec impact had no effect on ICP. BP and CPP were 10-15 mm Hg less than in the sham-injured animals throug hout the experiment (p < 0.05). With the 5 m/sec impact, ICP was trans iently increased for <15 min immediately after the impact. The ICP ret urned to preinjury levels by 30 min after the impact but then graduall y increased throughout the rest of the experiment, becoming significan tly greater than in the sham-injured animals by 5.5 h. BP and CPP were 10-15 mm Hg less than in the sham-injured animals throughout the expe riment (p < 0.05). LDF immediately decreased by 30% (p < 0.05) and the n gradually increased toward control values throughout the 8 h experim ent. The cortical impact model of TBI reproduces many of the hemodynam ic features of human head injury. Distinct cerebral hemodynamic patter ns are related to both the depth of deformation and the velocity of th e impact. This model may be useful for studying these manifestations o f TBI.