Journal of neurotrauma
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Journal of neurotrauma · May 1998
Moderate hypothermia for 48 hours after temporary epidural brain compression injury in a canine outcome model.
In a previous study with this dog model, post-insult hypothermia of 31 degrees C for 5 h prevented secondary intraventricular pressure (IVP) rise, but during 35 degrees C or 38 degrees C, one-half of the dogs developed delayed IVP rise to brain death. We hypothesized that 31 degrees C extended to 48 h would prevent brain herniation. Using epidural balloon inflation, we increased contralateral IVP to 62 mm Hg for 90 min. ⋯ The vermis downward shift was 6.8 +/- 3.5 mm in Group 1, versus 4.7 +/- 2.2 mm in Group 2 (p = 0.05). In an adjunctive study, in 4 additional normothermic dogs, hemispheric cerebral blood flow showed post-insult hypoperfusion bilaterally but no evidence of hyperemia preceding IVP rise to brain death. In conclusion, in this model, moderate hypothermia during and for 48 h after temporary epidural brain compression can maintain a low IVP during hypothermia but cannot prevent lethal brain swelling after rewarming and may cause coagulopathy and pulmonary complications.
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Journal of neurotrauma · May 1998
Relationship between severity of spinal cord injury and abnormalities in neurogenic cardiovascular control in conscious rats.
Abnormal sympathetic tone after spinal cord injury (SCI) initially results in hypotension and is subsequently associated with autonomic dysreflexia characterized by paroxysmal hypertension and bradycardia in response to noxious or visceral stimuli. To evaluate the effect of a clinically relevant compression model of SCI on cardiovascular control in the early postinjury period, we monitored arterial pressure (AP) and heart rate under control resting conditions and after visceral stimulation (colon distension) in conscious rats for 1 week after clip compression injury of the cord at T5. Rats were randomly allocated into 4 groups (n = 8 each): sham-operated, 20, 35, and 50 g injuries. ⋯ These data show that dysfunctional cardiovascular control after SCI is correlated with the severity of injury. Mild and moderate compressive SCI result in transient cardiovascular abnormalities which normalize by 1 week. In contrast, more severe injuries are associated with neurogenic hypotension and autonomic dysreflexia.