Intracranial hypertension and brain oedema in albino rabbits. Part I: Experimental models.

Three models of experimental cerebral oedema in rabbits are described, one producing vasogenic oedema with a cold lesion, the other producing a cytotoxic cerebral oedema with a metabolic inhibitor, 6-aminonicotinamide (6-ANA), and finally a model employing in the same animal both vasogenic and cytotoxic injuries. The following parameters were assessed: behaviour, EEG, intracranial pressure (ICP), cerebral elastance (Em), blood brain barrier integrity, brain water, electrolyte content, and volume change. Behaviour was normal in the cold lesion group, was abnormal following the administration of 6-ANA, and pronouncedly abnormal in animals with a combined lesion. Mean ICP (PaCO2 37 +/- 42 torr) in the control group was 2.7 +/- 2 torr, in the cold lesion group 8.4 +/-6, in the 6-ANA group it was 8.7 +/- 4, and in the combined lesion group 15.8 +/- 8 torr. Em for the control group was 2.6 +/- 1.3 torr, in the cold lesion group it was 5.6 +/- 4 torr, in the 6-ANA group it was 8.8 +/- 5 torr, and in the combined lesion group it was 8.0 +/- 4 torr. The 6-ANA group manifested oedema that involved primarily the grey matter. In the control animals grey matter water content was 79.99 +/- 0.8%, and in the 6-ANA group it was 81.73 +/- 0.9% (P less than 0.001). A group had both grey and white matter content measurements under the area of a sham lesion, and this was 79.2 +/- 1.3% for the left hemisphere and 79.1 +/- 1.3% for the right. Following a cold lesion of the left hemisphere, the water content was 81.85 +/- 1% (P less than 0.005), and 80.25 +/- 1% (P less than 0.01) in the unlesioned right hemisphere. In those animals with combined cold lesion and 6-ANA administration, the water content of the left hemisphere increased to 82.8 +/- 1% (P less than 0.05 from vasogenic oedema alone), and in the right hemisphere to 81.1 +/- 1% (P less than 0.5 from vasogenic oedema alone).