Extracellular space and electrolyte distribution in cortex and white matter of dog brain in cold induced oedema

Abstract

Summary24 hours after a circumscribed cold injury of the cortex dog brains were perfused from the lateral ventricle and the frontal subaraehnoidal space to the eisterna magna with an artificial CSF containing trace amounts of 35S-labelled thiosulphate. Simultaneously the extraeellular tracer was administered intravenously.Extracellular fluid volume was estimated and found to be increased from 10 to 15% in the oedematous cortex and from 10 to 27% in the oedematous white matter. The actual size of ECS in oedematous white matter, however, must be larger as indicated by the relative alterations of thiosulphate distribution, tissue water, sodimn and chloride. Apparently a small part of the fluid accumulation affects the cellular compartment in oedematous white matter. It may be concluded from the close spatial correspondence of the spreading of 1181 albumin mad Evans blue, the increase in water and sodium content, and the enlargement of the TSS that the dilated extraeellular channels are filled with a plasma like oedema fluid, derived from blood.The oedema resulting from a local cold injury to the cortex produces all experimental model bearing similarities to the oedema following traumatic brain injury. This model has often been used to study the disturbance of blood-brain barrier to various compounds 3, G, 11, 13, 14 as well as the morphological 3, 4, 5, 15, 22 and chemical changes 3, 6, 16 that occur in oedematous tissue. In contrast, the sequence of events oeeuring during the formation of oedema and the physiochemieal forces (in terms of diffusior~ and driving forces) involved in the formation and resolution of brain oedema are not adequately kaowm Of

Heterogeneity of aquaporin-4 localization and expression after focal cerebral ischemia underlies differences in white versus grey matter swelling

“…Interestingly, we found that cortical grey matter and subcortical white matter exhibit greatly different propensities for tissue swelling after cerebral ischemia. After ischemia, the ipsilateral cortical grey matter was swollen by 8.95 % ± 2.64 % compared to the contralateral cortex, while the ipsilateral subcortical white matter was swollen by a remarkable 42.5 % ± 8.84 %.These findings are in alignment with data from prior studies showing that white matter is highly susceptible to swelling after acute CNS injury [ 25 , 26 ]. There are at least two possible mechanistic explanations for the striking swelling exhibited by subcortical white matter: firstly, for reasons yet to be clarified, subcortical white matter may be more susceptible to the formation of edema fluid than cortical grey matter; secondly, subcortical white matter might be simply serving as a sink for edema fluid generated elsewhere [ 70 ].…”

“…Given that the human prefrontal cerebrum is ~2/5ths white matter [ 23 ], white matter integrity after stroke is a stronger functional predictor than preserved neurological function [ 24 ]. Insofar as certain studies indicate that white matter is highly susceptible to swelling after acute CNS injury [ 25 , 26 ], it is important to determine whether astrocyte regional heterogeneity manifests as significant differences in certain molecular events that drive cerebral edema formation.…”

The Pattern of AQP4 Expression in the Ageing Human Brain and in Cerebral Amyloid Angiopathy

“…White matter hyperintensities (WMH) [2] and abnormalities in fluid homeostasis in the white matter are frequent radiological observations in neurodegenerative diseases. White matter is highly susceptible to oedema after acute injury to the central nervous system (CNS) [27][28][29] and WMH are a common finding on computer tomography (CT) or magnetic resonance imaging (MRI) in the elderly, in stroke, dementia and cerebral amyloid angiopathy (CAA) [30]. Dilated perivascular spaces visible on MRI have been described in the white matter of patients with Alzheimer's disease (AD) or CAA [31].…”

Role of pressure gradients and bulk flow in dynamics of vasogenic brain edema

“…,2~ In vasogenic brain edema associated with brain injury, tumor, or inflammation, the ECS is significantly enlarged) , 9,19,21 These dilated spaces may provide a pathway for the movement of edema fuid. The two mechanisms by which the edema fluid and its constituents might spread through these spaces are diffusion and bulk flow) 6,27 These two possible processes may be identified by their distinctive properties.…”