Measurements of regional cortical blood flow during changes in extracellular potassium activity evoked by direct cortical stimulation in the primate.
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Biomedical subjects
Publications and source records attributed to L Symon.
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Following the massive increase in extracellular potassium activity that occurs in cerebral cortex when local blood flow falls below 8--11 ml/100 g/min, recovery of potassium toward normal levels might be expected when flow is restored. This study assessed the reversibility of such potassium increases, produced by middle cerebral artery occlusion in 13 baboons anaesthetised with alpha-chloralose, in relation to a wide range of ischaemic duration and density and post-occlusion flow. Potassium was measured with ion-exchanger microelectrodes and flow by hydrogen clearance. The artery was occluded for 136 +/- 63 min (mean +/- SD) and measurements were continued thereafter for 93 +/- 57 min without systemic hypertension. Upon reperfusion, partial or complete recovery (i.e., to within control confidence limits) of potassium was seen in all animals, but the rate of recovery varied widely and potassium clearance showed bi-compartmental characteristics in 7 animals. The fast component (or initial slope) rate constant was significantly correlated with post-occlusion flow and (inversely) with the duration of occlusion for which flow fell below the arbitrary threshold of 10 ml/100 g/min (the flow deficit). The slow component was unrelated to these quantities. Complete recovery was associated with a significantly higher post-occlusion flow, and smaller flow deficit, than was partial recovery. Secondary increases in potassium, associated with relatively high flow deficits and post-occlusion flows, were seen in 5 animals. These results are discussed in terms of factors that may determine potassium clearance and the possibility that elevated levels of potassium (demonstrated here to be prolonged well into the post-occlusion phase) might influence the evolution of a cortical infarct.
Tinofedrine, a new derivative of l-norephedrine, was examined for cerebral vasodilator activity in man. Ten patients with reduced cerebral blood flow (CBF) and multi-infarct dementia were given the drug intravenously. Cerebral blood flow increased significantly by 28% from a mean of 43.3 to 55.5 ml/100 g/min.
Six patients with cerebral arteriovenous malformations which did not show any pathological circulation at angiography are described. Computed tomogram appearances of such lesions may be difficult to distinguish from tumours. The need for surgical exploration in localised high attenuation lesions of uncertain nature is stressed, and the literature is reviewed.
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Cerebral blood-flow (C.B.F.) was measured in 38 patients with haematocrit values (Hct) in the range 0-47--0-53 and was found to be significantly lower than in 43 patients with Hct in a lower range (0-36--0-46). After reduction of Hct in the higher Hct group by venesection, flow increased by a mean of 50%. This improvement in flow was largely due to a reduction in viscosity. Hct around the generally accepted upper limit of normal may be an important factor in the causation of occlusive vascular disease.
Cerebral blood-flow (C.B.F.) has been measured in 16 patients with polycythaemia of differing severity. The mean C.B.F. was 37-9 ml/100 g/min, which is significantly below the normal level of 69-1 (S.D. 9-3) ml/100 g/min (P less than 0-001). C.B.F. measurement was repeated after venesection in 15 of the patients. Lowering the haematocrit from a mean of 0-536 to a mean of 0-455 was associated with a 73% increase in mean C.B.F. (P less than 0-001) and a 30% reduction in whole-blood viscosity. Low C.B.F. was found at haematocrit levels between 0-46 and 0-52. Haematocrit levels that are currently acceptable in the management of polycythaemia may therefore be too high.
Many neuroradiological procedures are available for the elucidation of lesions presenting with clinical evidence of a cerebellopontine angle syndrome. For 10 years we have favoured plain skull rays, sometimes supplemented by gamma encephalography, followed by angiography and have uncommonly needed further information from other contrast studies before operation. The innocuous value of computed tomography (C.T.) made it necessary to consider modification of this routine which had been found to be very satisfactory in routine practice. To obtain precise information on the diagnostic reliability and complications of the method we reviewed a large consecutive series of patients presenting with angle lesions. The radiological signs in such cases have been described many times and are well known, but our findings in a single comprehensive series emphasize the value of the method and are presented in a review. The modifications induced by CT are discussed.
Extracellular K+ activity (Ke), local tissue blood flow and the cortical evoked potential (EP) were measured concurrently in the cerebral cortex of baboons anaesthetised with a-chloralose. Flows were progressively reduced from normal by occlusion of the middle cerebral artery and controlled steps of exsanguination. Our data suggest that 3 stages may be identified in the disturbance of K+ homeostasis produced by progressive ischaemia. In the first stage, at flow levels similar to those sufficient to abolish the EP (12-16 ml/100 g/min), small, self-limiting increases in Ke occur, probably reflecting K+ efflux into the extracellular space (ECS) with partial impairment of K+ clearance from the ECS. The second stage occurs at distinctly lower (P less than 0.01) levels of flow (8-11 ml/100 g/min), and is characterized by a massive (30-80 mM) increase in Ke, which we attribute to an increase in ionic permeability of cell membranes with further impairment or overloading of K+ clearance mechanisms. In the third stage, at flows below about 6-8 ml/100 g/min, the data indicate an inverse relationship between flow and Ke with persisting high Ke levels, suggesting complete loss of K+ clearance. Transient increases of Ke also occur in the flow range 4-13 ml/100 g/min, the rate of recovery of Ke in their decay phase being positively corelated with flow (P less than 0.005).
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Cerebral blood flow (CBF) was measured before and after intravenous injection of the cerebral vasodilator nicergoline in 13 patients with cerebrovascular disease. CBF increased in seven. The possibility that the effect of the drug in the remainder may have been masked by a fall of CBF which occurs during sequential measurement of patients at rest is discussed.
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