Abstract
Intracranial pressure (ICP), blood pressure (BP), cerebral perfusion pressure (CPP), and cortical perfusion (LDF) of the contralateral parietal cortex were measured after cortical impact injury in 36 rats. Changes in these physiologic parameters were compared using analysis of variance 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 kept constant, and the severity of the injury was determined by varying the depth of cortical deformation from 2 to 3 mm. The peak pressure inside the skull was directly related to the depth of cortical deformation, 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 increased throughout the 8 h experiment, becoming significantly greater than the sham-injured animals by 5 h after the impact. LDF gradually returned toward normal throughout the experiment. With the 3 mm depth injury, 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 min, 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-injured animals for the rest of the experiment. LDF decreased by an average 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 was kept constant at 2.5 mm, and the severity of the injury was determined by varying the velocity from 1 to 5 m/sec. The peak ICP was significantly 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, respectively. 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-injured 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 throughout the experiment (p < 0.05). With the 5 m/sec impact, ICP was transiently in creased for <15 min immediately after the impact. The ICP returned to preinjury levels by 30 min after the impact but then gradually increased throughout the rest of the experiment, becoming significantly 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 experiment (p < 0.05). LDF immediately decreased by 30% (p < 0.05) and then gradually increased toward control values throughout the 8 h experiment. The cortical impact model of TBI reproduces many of the hemodynamic features of human head injury. Distinct cerebral hemodynamic patterns are related to both the depth of deformation and the velocity of the impact. This model may be useful for studying these manifestations of TBI.
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