Abstract

Background After severe burn, the effective circulating blood volume decreases drastically due to massive body fluid loss, and blood redistribution occurs to maintain sufficient blood supply to vital organs. Blood perfusion of brain tissue changes and the permeability of the blood brain barrier increases due to ischaemia and hypoxia, which results in brain oedema. The goal of this study was to explore the changes of cerebral blood flow during the brain oedema at the early stage of severe burn. Methods Twenty-six dogs were randomly divided into control and 6, 12, 18, and 24 PBH groups. The manifestation of MRI and histopathology, changes of brain water content were investigated; the shapes and distribution of the cerebral capillaries were observed with the endogenous AKP histochemical staining method and image analysis technique. The volume, surface, and length fractions of cerebral capillaries were tested and analysed with a stereographic method in each group, respectively. Results The earliest changes of cerebral oedema were found at 12 PBH with MRI, which showed the brain swelling as characteristic of cerebral morphological changes. The decrease of SIR on T 1WI was not observed until it was above 10%. Signal of T 2WI increased for 8.29% at 24 PBH. Histological changes were observed as early as 6 h after burn, accompanied by swelling of endothelial cells and peri-vascular astrocytes, vacuolation took place in neurons at 12 h after burn, necrosis of different degrees in capillary endothelium, neurons, and axons. Increase in cerebral water content was noted at 6 h postburn, and it was the most marked in 24 postburn group.The distributional density of capillaries became thicker at 6 h and 12 h postburn, the shapes were normal. The capillaries became sparser at 18 h, and almost disappeared from view, only a few ends of capillaries in the shape of vine were seen at 24 h postburn. The percentages of capillary volume, surface, and length fractions were increased at 6 h and 12 h, but decreased at 18 h and reached the lowest point at 24 h postburn ( P < 0.05). Conclusion We suggest that the changes of cerebral blood flow might play an important role in the pathogenesis of brain oedema in the early stage of severe burn.

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