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  • Title: [Importance of the study of cerebral blood flow and regional oxygen consumption in cerebral ischemia].
    Author: Clanet M.
    Journal: Presse Med; 1987 Jun 18; 16(23):1135-8. PubMed ID: 2955353.
    Abstract:
    Studies of experimentally-induced ischaemia have shown that the intensity of neuronal suffering is related to the fall in perfusion rate. Below a certain level, called functional threshold, cerebral function is reversibly altered, whereas at a lower level (tissue necrosis threshold) the damage inflicted on neurons is irreversible. Between these two threshold lies a "penumbra zone". This concept of thresholds must be mitigated by 2 parameters: duration of ischaemia and selective vulnerability of the various structures affected. Variations in blood flow rate only indirectly affect the state of tissues. Techniques developed from positron emission tomography make it possible to evaluate the metabolic activity of brain tissue in vivo: oxygen consumption (CMRO2), oxygen extraction (EO2) and glucose consumption (CMRG) which are thus correlated to cerebral blood flow and cerebral blood volume, sometimes also to tissue pH. Normal relations between blood flow rate and metabolism may be altered. Misery perfusion reflects a fall in cerebral blood flow with an increase in EO2 and often a decrease in CMRO2, whereas luxury perfusion reflects an increase in cerebral blood flow rate with reduction of CMRO2, EO2 and CMRG. The type of alteration encountered in human ischaemia varies according to the nature of the accident: studies of transient accidents emphasize the different haemodynamic aspects of occlusion of the wider arteries. The metabolic and haemodynamic profiles of established ischaemic accidents vary according to their type and to the time of the study, reflecting the complexity of the physiopathological mechanisms involved; they are frequently associated with metabolic repercussions at a distance from the ischaemic focus, which supports the concept of diaschisis. Arteriopathic dementia probably does not result from chronic ischaemia of the cerebral parenchyma.
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