A Remington humane stunner was used to deliver blows to the skulls of anesthetized cats. The animals were sacrificed at 30 minutes or 1, 2, or 6 hours after trauma and selected for data collection on the basis of the following two categories of gross intracranial pathology: 1) unilateral contusion, with subarachnoid hemorrhage (SAH); or 2) SAH only. For selected cats, specific gravity was measured in 5- to 10-mg samples of uncontused tissue taken from coronal slices at the level of the frontoparietal suture. The regions tested included dorsal cerebral cortex, subcortical white matter, deep white matter, and caudate nucleus. Specific gravity data from injured animals were compared with those from similar areas in uninjured anesthetized cats to test for cerebral edema. At 30 minutes after head injury, contused hemispheres had significant edema of all tested except the caudate nucleus. Edema of the subcortical and deep white matter increased with time after the injury. Increase in water content of the cerebral cortex was transient and appeared unrelated to contusion. The caudate nucleus was edematous only at 6 hours, suggesting movement of fluid from the deep white matter compartment into the nucleus. The hemispheres opposite the contusion and those related to SAH had, with one exception, an absence of edema in the white matter and caudate nucleus, but a transient increase in water content of the cerebral cortex. These findings suggest that, in the presence of contusion, cerebral edema can contribute to brain swelling as early as 30 minutes after closed head trauma. In addition, a transient and minimal cortical edema, perhaps related to ischemia, occurred in all groups of hemispheres examined.
A Remington humane stunner was used to deliver a blow to the left side of the surgically-exposed skull in ketamine-anesthetized cats. At 15 minutes after the trauma, brain tissue was frozen in situ. In animals without visible tissue hemorrhage (Grade 0) and in those with unilateral cerebral contusions involving the cerebral cortex and white matter (Grade 2), regional cerebral metabolite concentrations were measured by enzymatic-fluorometric techniques and edema was tested with an organic gradient. No substantial changes in cerebral metabolite concentrations were observed in head-injured animals without cerebral contusions. In animals with unilateral contusions, the white matter neighboring the tissue hemorrhage had an increase in lactic acid and a decrease in phosphocreatine as compared to values from corresponding areas on the contralateral side, and in control and Grade 0 animals. The cerebral cortex adjacent to tissue hemorrhage had a variable response that ranged from metabolite concentrations within normal ranges to marked decreases in high-energy phosphates and increases in lactic acid. Metabolites of the cortex and white matter contralateral as well as distant to contusion were not statistically different from values of control animals. Changes in several metabolites correlated well with the magnitude of edema. It is concluded that focal metabolic alterations can occur shortly after severe blunt head injury, and that these events may contribute to acute traumatic cerebral edema.
To evaluate the location and early time course for development of cerebra edema following therapy for diabetes, streptozotocin-diabetic rats were subjected to constant i.v. infusion with saline and regular insulin. At the end of 1, 2, and 5 h of therapy, these rats were killed and tested for density of the cerebral cortex, subcortical white matter, caudate-putamen, thalamus, and medulla. Density data from treated animals were compared with those from control animals. From these data, change in brain tissue volume as water was calculated. Diabetic animals killed after 1 h of fluid and insulin therapy demonstrated a modest increase in brain water content of all areas tested except white matter. Following 2 h of therapy, all regions tested were edematous, with a magnitude of edema that was similar to that seen at 1 h. After 5 h of therapy, there was further increase in water content of the cerebral cortex, but not the other regions examined. Treatment with saline alone did not result in central overhydration. The findings of this study suggest that aggressive therapy with fluids and insulin, but not fluid alone, results in global overhydration of the brains of diabetic animals. Prolonged fluid and insulin treatment with a return of blood glucose to normal values causes further and preferential accumulation of edema fluid in the cerebral cortex.
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