TY - JOUR
T1 - Focal microvascular occlusion after acute subdural haematoma in the rat
T2 - a mechanism for ischaemic damage and brain swelling?
AU - Fujisawa, H.
AU - Maxwell, W. L.
AU - Graham, D. I.
AU - Reasdale, G. M.
AU - Bullock, R.
PY - 1994
Y1 - 1994
N2 - Using a rat model of subdural haematoma (SDH) which is associated with ischaemic damage in the ipsilateral hemisphere, we have studied the microcirculation and the time course of development of ischaemia beneath the subdural haematoma. The latter was investigated by measuring cerebral blood flow (CBF) using the hydrogen clearance technique, the former by electron microscopy (EM) and carbon black angiography. CBF fell below 5 ml/100g/min within five minutes of SDH and remained low (< or = 7 ml/100g/min) for over two hours. Contralateral CBF fell to 54% of control but normalized by 1 hour. Carbon black angiography showed absent perfusion beneath the SDH. EM demonstrated: 1) normal cortical vessel traversing the haematoma; 2) occlusion of cortical vessels under SDH by clotted red cells and platelets; 3) massively enlarged perivascular spaces due to swelling of astrocytes. No vasospasm was seen. The "ischaemic core" may develop where microvascular occlusion occurs, and this microcirculatory disturbance initiates ischaemic cell damage with release of glutamate, which spreads outward from the core. This causes further damage of neurons and swelling of astrocytes, resulting in severe ischaemic necrosis, and progressive brain edema. The cause of microvessel occlusion remains unknown.
AB - Using a rat model of subdural haematoma (SDH) which is associated with ischaemic damage in the ipsilateral hemisphere, we have studied the microcirculation and the time course of development of ischaemia beneath the subdural haematoma. The latter was investigated by measuring cerebral blood flow (CBF) using the hydrogen clearance technique, the former by electron microscopy (EM) and carbon black angiography. CBF fell below 5 ml/100g/min within five minutes of SDH and remained low (< or = 7 ml/100g/min) for over two hours. Contralateral CBF fell to 54% of control but normalized by 1 hour. Carbon black angiography showed absent perfusion beneath the SDH. EM demonstrated: 1) normal cortical vessel traversing the haematoma; 2) occlusion of cortical vessels under SDH by clotted red cells and platelets; 3) massively enlarged perivascular spaces due to swelling of astrocytes. No vasospasm was seen. The "ischaemic core" may develop where microvascular occlusion occurs, and this microcirculatory disturbance initiates ischaemic cell damage with release of glutamate, which spreads outward from the core. This causes further damage of neurons and swelling of astrocytes, resulting in severe ischaemic necrosis, and progressive brain edema. The cause of microvessel occlusion remains unknown.
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U2 - 10.1007/978-3-7091-9334-1_52
DO - 10.1007/978-3-7091-9334-1_52
M3 - Article
C2 - 7976543
AN - SCOPUS:0028189686
VL - 60
SP - 193
EP - 196
JO - Acta Neurochirurgica, Supplement
JF - Acta Neurochirurgica, Supplement
SN - 0065-1419
ER -