Histopathological and enzyme-histochemical changes after brain compression (author's transl)

Abstract

Effects of compression of the brain at various pressures were studied histopathologically and enzyme-histochemically. Sixty two adult mongrel dogs were used under general anesthesia with pentobarbital sodium. After craniotomy, the frontal lobe was compressed for an hour directly by a plastic disc 10 mm in diameter, which was connected to a spring. (1) Degree of brain damage under various compression pressures. Eighteen dogs were divided into three groups. For each group, the brain was compressed with pressures of 60 mmHg, 100 mmHg and 240 mmHg respectively. The brains compressed with a 60 mmHg pressure showed vasogenic brain edema histopathologically. Those with a 100 mmHg pressure showed mainly softening and necrosis due to venous infarction and they were dominant in the white matter. The brains compressed with 240 mmHg demonstrated venous infarction and hemorrhagic infarction secondary to pericapillary diapedetic hemorrhage. (2) Effect of subarachnoid hemorrhage on the compressed brain. In eight dogs, 1 ml/kg of autogenous blood was injected into the cisterna magna. Two days later, these dogs underwent brain compression under 240 mmHg of pressure. Histopathologically the brains showed no significant differences compared to the brains without subarachnoid hemorrhage which were compressed with the same pressure. (3) Effect of cortical vein section on the compressed brain. In 12 dogs, bridging veins were sectioned before brain compression with 240 mmHg of pressure. Five of them showed macroscopic hematomas predominant in the white matter. Seven of them showed microscopic hemorrhage. In another five dogs, bridging veins were sectioned but compression was not performed. Two of them showed only scattered pericapillary hemorrhage without hematoma or infarction. The rest showed neither edema, infarction nor hemorrhage. These data demonstrated that disturbance of the venous return aggravated the degree of brain damage by brain compression, and suggested that bridging veins should be preserved whenever possible during any operation. (4) Enzyme-histochemical changes were investigated with phosphorylase (P-Pase), glucose-6-phosphate dehydrogenase (G6PD), lactate dehydrogenase (LDH), alkaline phosphatase (Al-Pase). adenosine triphosphatase (ATPase) and cytochrome oxidase (Cyt. ox.). The infarcted area showed decreased activities of all these enzymes except LDH in some cases. Edematous and peri-infarctic areas demonstrated increased activities of P-Pase, G6PD and LDH in the astroglial cells, and increased Al-Pase in the capillary walls, but decreased activities of ATPase and Cyt. ox. in the astroglial cells. These enzyme-histochemical findings indicated increased aerobic glycolysis, disturbed metabolism in the mitochondria, and permeability changes in the astroglial cells and the capillary walls, mainly due to the impaired blood-brain barrier. (5) Effects of therapeutic agents were investigated by the enzyme-histochemical technique in 19 dogs. Ten percent glycerol (5 ml/kg/day i.v.) reduced the activity of G6PD and increased the activity of LDH and ATPase. Glycerol seemed to be utilized to preserve enzyme activity and energy metabolism. Dexamethazone (2 mg/kg/day i.m.) increased the activity of LDH which could accelerate the glycolysis. Therefore it had the effect of improving the metabolism. Dimethyl sulfoxide (DMSO, 4 ml/kg/day i.v.) had no effect on the compressed brain. Histopathologically, however, these three agents had no effect on the infarcted brain.