1. MRI scanning method and image analysis

The type of MRI employed in this study was 0.2T open style permanent magnets. A spin-echo sequence with T1WI (TR/TE 560/30 ms) and T2WI (TR/TE 6000/114 ms) was set. The matrix of imaging was set at 256 x 256 and the field of view at 200 mm. Nine contiguous sections with 4 mm thick slices were harvested in each sequence. Regular regions (0.3 cm2/ROI) were selected from both sides of the frontal lobe, the parietal lobe cortices, the basal ganglion, the cerebellum, and the brain stem areas for image analysis. The mean signal intensity of TIWI and T2W 1 in ROI from different layers, and the subcutaneous normal soft tissue of the corresponding layers was measured. The ratio of the above two measurements was set as standard signal intensity ratio (SIR).

            2. Pathomorphological study

a. Gross examination. The purpose was to observe the colour; distribution, and running patterns of cerebral vessels and the surface forms of various cerebral tissues.

b. Light microscopy (LM) examination. The harvested brain tissue was fixed in 10% formalin solution for one week. Samples sized 5 mm3 obtained from both sides of the frontal lobe,, parietal lobe, cortices, cerebellum cortices, brain stem, and basal ganglion were gradiently dehydrated with ethanol, embedded with paraffin, sliced, and then stained with haemotoxylin-eosin.

c. Electron microscopy examination. One cubic mm brain tissue samples were harvested from both sides of the frontal lobe and the parietal lobe cortices respectively under anaesthesia and placed in 3% glutaraldehyde for routine fixation for 6 h. The samples were then dehydrated gradiently with acetone, embedded, sliced, stained, and finally examined using a transmission electron microscope (EM).

'The ANOVA statistical analysis and Student's t test were. employed. The data were expressed as mean ± standard deviation (y ± S).

Results

1. Comparative observation of brain with MRI and pathomorphology

Control group. TIWI of MRI scanning revealed a normal-size brain figure and a clear structure of the cerebral sulci, cracks, cisterns, and ventricles. The TZW1 signal revealed a clear boundary between grey matter and white matter. Gross and microscopic examination of brain tissue appeared normal.
Simple burn group. MRI scanning revealed little change at PBH 6. It was shown by LM that the capillary was slightly dilated and hyperaemic. The pericapillary gaps were slightly broadened. The neurons exhibited dissolution of the Nissl bodies and karyopyknosis. EM examination revealed hypertrophy of the capillary endothelia and swelling of the end foot of the astrocyte.
TIWI in two dogs at PBH 12 indicated shallower cerebral sulci and tracks and slightly narrower cerebral cisterns and ventricles. T2W 1 showed an obscure boundary between grey and white matter. Observation of the brain tissue with LM indicated the above lesion became more obvious than at PBH 6. EM examination showed swelling of the perivascular astrocyte end foot and cracks in the mitochondrial crista. Gross examination found slight expansion, congestion, and normal running of external cerebral vessels.
Burn with sodium lactate group. MRI scanning and pathomorphological findings at PBH 6 were similar to those in the SB group. MRI revealed relative normal brain parenchymal figures, structure, and signals at other time points. At time points later than PBH 12, examination with LM indicated changes of capillary endothelia and nerve cells similar to those at PBH 6. In addition to the results observed at PBH 6 with EM, it was found that part of the basement membrane became thicker and looser. At PBH 24, mitochondrial lysis and disappearance were observed.
Burn with glucose solution group. The results of MRl scanning and pathomorphological examination at PBH 6 showed no obvious difference from those in other groups (Figs. 1, 2).
There were however gradual morphological changes in the brains of two dogs at PBH 12, three at PBH 18, and four at PBH 24 on MRI scanning. TIWI indicated symmetrical enlargement of the cerebral parenchyma, flattening and disappearance of cerebral sulci and cracks, and narrowing and closing of cerebral cisterns and ventricles. T2W 1 showed a mild diffuse increase in the signals in cerebral parenchyma and partial disappearance of the boundary between grey and white matter in two dogs at PBH 24 (Figs. 3, 4). It was found that cerebral endothelia exhibited collapse, defect, and enlargement of partial interendothelial connective gaps on EM examination. Increased meninx tension, widened gyri, and shallowed cerebral sulci were noted on gross examination at PBH 18 and 24.
When inspected by LM, the brain white matter exhibited lysis and disappearance, and the neurons revealed karyopyknosis, etc. On EM the mitochondria of the capillary endothelia swelled and the mitochondrial crista were fractured and deranged. Swelling of the karyon, margination of chromatin, capillaries were dilating, tortuous, and hyperaemic. The neurons revealed vacuolization and they aggravated with the lapse of time on LM examination (Fig. 5). Capillary irregularity of the capillary basement membrane, and obvious vacuolar swelling of the end foot of the astrocyte were also observed (Fig. 6).

Fig. 1 - The cerebral sulci, cracks, cisterns, and ventricles of the brain appeared normal at PBH 6 in glucose solution group (Ti-weighted MRI, coronal section). Fig. 2 - The boundary line between grey matter and white matter appeared clearly, and there was no abnormal cerebral signal at PBH 6 in the glucose solution group (T2-weighted MRI, coronal section). Fig. 3 - The cerebral sulci and cracks became flat and tended to disappear; the cerebral cisterns and ventricles were narrowed and blocked at PBH 24 in the glucose solution group (Ti-weighted MRI, coronal section). Fig. 4 - It was difficult to distinguish grey matter from white matter at the boundary line; the brain signal was not uniform at PBH 24 in the glucose solution group (T2-weighted MRI, coronal section). Fig. 5 - Evident enlargement of the perivascular gaps and a compressed capillary lumen were found at PBH 24 in the glucose solution group (LM, HE x 400). Fig. 6 - Swelling of mitochondria of capillary endothelia and vacuolation of perivascular end foot were observed at PBH 24 in the glucose solution group (TEM x 8000).

2. Changes of SIR in MRI
TIWI SIR decreased by 5.1%, while T2WI SIR increased by 7.39% at PBH 12 in the SB group. There was no significant change of SIR in the BSL group. However, in the BGS group, TIWI SIR decreased by 10.39% (p < 0.05), while T2W 1 SIR increased by 8.29% (p < 0.05) at PBH 24 (Tables I, II).

Discussion

The results of this study indicate that after the infusion of a 5% glucose solution based on the Parkland formula at PBH 6 brain oedema developed in dogs with typical pathological features and prolongable survival time, which thus provided a reliable and optimal model of brain oedema in the early stage after severe burn for MRI study. The dogs in this group revealed brain swelling on MRI examination at PBH 12, which was most evident at PBH 24.
The pathomorphological changes of brain oedema started at PBH 6 and aggravated with the passing of time, and they were consistent with the MRI scanning results. However, positive MRI findings were observed after the path omorphological changes. In this study, positive MRI findings appeared only after PBH 12.
The pathomorphological changes of early post-bum brain oedema possessed characteristics of both vasogenic and cellulartoxic oedema with similar features in the MRI findings. Encephalaemia and vasogenic oedema were the main MRI findings in brain tissue before P13H 12. The brain tissue was found to be hyperaemic with increased permeability of the blood brain barrier, widened capillaries, and perineurocytic gaps at P13H 6. Endothelial cells and neurons revealed swelling by pathomorphological study after PBH 12. At PBH 24 we observed attenuated capillary hyperaemia and dilatation, flattened cerebral sulci and cracks, and increased tension of the meninges.
The results implied that cellulartoxic brain oedema dominated the middle and late period of the formation of early post-burn brain oedema. Cellulartoxic and vasogenic oedema may be a common cause of the morphological changes of brain tissue and it may also be the pathological basis of the aggravation of brain oedema after PBH 12. MRI signal intensity can be applied to make a quantitative analysis of the changes in brain oedema caused by trauma, ischaemia and hypoxia, tumour, and cerebritis.
In our experiment, MRI signal intensity of the brain tissue in the early stage post-burn was analysed quantitatively. The results indicated that the TjWI SIR of brain tissue was slightly decreased before PBH 18 and manifestly decreased at PBH 24 compared with that of the control group. T2WI SIR was slightly enhanced in 40% of all the dogs at P13H 24. There was not so much alteration of MRI SIR at PBH 12 in the SB group, owing to the relatively short period of observation.
Also, there was no abnormal MRI scanning at P13H 6 in the SL group, owing to the optimal control of shock. Dynamic observation of MRI SIR in the GS group found that signal intensity changes could not be detected before a 10% decrease in TIWI SIR, which implied that the pathomorphological changes in brain oedema had already occurred when TjWI SIR decrease was detected. It was observed that MRI signal intensity could to some degree reflect the degree of diffusion of the oedematous fluid of early post-burn brain oedema, but this was not well correlated with changes in pathomorphology and the trend of MRI morphological changes.
The changes in MRI signal intensity were related not only to those of brain water content but also to changes in the dynamic structure of brain tissue water and existing status, magnetic field strength, proton density, scanning condition, etc. MRI intensity changes may therefore play a role in reflecting the pathomorphological changes of post-burn brain oedema, which is a special type of brain oedema.
In conclusion, MRI and pathomorphological comparative studies were employed in the observation of an animal model (dogs) with brain oedema in the early stage after severe burn. This may be considered to be a related procedure for the diagnosis and treatment of post-burn brain oedema, aimed at improving the outcome of brain oedema management after severe burn.

RESUME. Cinquante-deux chiens ont ete divises en maniere randomisee dans un groupe t6moin, un groupe de brulures simple lBS), un groupe de brulures traitees avec le lactate de sodium (BLS), et un groupe de br6lures traitees avec une solution de glucose i BSG). Les manifestations des chiens dans le groupe temoin ont ete confrontees avec celles des groupes des animaux br616s dans les premiere phases (6, 12, 18 et 24 h) apres une brnlure severe (50% de la surface corporelle totale de troisieme degre), avec Vemploi de la resonance magnetique nucl6aire (RMN) et Fobservation pathologique (aspect grossier, microscope simple, microscope electronique). La premiere indication d'oedeme c6rebrale se manifestait 12 h apres la br6lure dans le groupe BSG, qui presentait Fenflure cerebrale comme caracteristique de la RMN. La diminution du rapport de Fintensite du signal (RIS) sur TIWI n'a pas ete observee avant d'atteindre 10%. Le RIS sur T2WI augmentait de 8.29% (p < 0,05) a 24 h apres la bru"lure. 11 etait difficile de distinguer entre la matiere grise et la matiere blanche a la ligne de delimitations, qui n'etait pas visible en suite. Les transformations histologiques de 1'oedeme c6r6brale ont ete observees des la sixieme heure apres la bralure, accompagnees par une enflure des cellules endovasculaires. Le phenomene de la vacuolation a ete observe dans les neurones a 12 h apres la brulure, comme aussi tme n6crose isch6mique de degre variable de 1'endothelium capillaire, des neurones et des axones. Ces modifications devenaient plus marquees dans le temps. Le groupe BSG pr6sentait les consequences les plus evidentes a 24 h apres la brulure. Les resultats indiquent que le modele employe d'oedeme cerebrale apres la brulure severe pr6sentait les caracteristiques de Foedeme vasogenique et de Foedeme celluliaretoxiiique dans 1'examen RMN et pathologique