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A J Strong

Publications and source records attributed to A J Strong.

At least 55 records · Page 3Linked to original sources

The cortical ischaemic penumbra associated with occlusion of the middle cerebral artery in the cat: 1. Topography of changes in blood flow, potassium ion activity, and EEG.

The gyral topography of the ischaemic penumbra associated with middle cerebral artery occlusion was studied in cats; local blood flow (hydrogen clearance, 2-min initial slope analysis), pial surface potassium activity (Kp), and electroencephalogram (EEG) amplitude were recorded on the ectosylvian, suprasylvian, and marginal gyri. Penumbral conditions were defined as a reduction of EEG amplitude in the absence of a major increase in Kp. Whole hemisphere cerebral blood flow prior to occlusion was 35.6 +/- 11.4 (SD) ml 100 g-1 min-1 (n = 25), and fell significantly (p less than 0.001) to 13.0 +/- 4.7 (SD), 14.1 +/- 6.6, and 23.8 +/- 9.3 on ectosylvian, suprasylvian, and marginal gyri, respectively. Pre-occlusion Kp was 3.0 +/- 0.9 mM (n = 53); sustained, steady-state increases in excess of 11.5 mM occurred in 5 of 7 (71%) experiments on ectosylvian gyrus, in 13 of 22 (59%) experiments on suprasylvian gyrus, and in 2 of 24 experiments on marginal gyrus. Transient increases in Kp occurred at occlusion and resolved to baselines significantly higher than control in 5 (23%) experiments in suprasylvian gyrus and in 15 (63%) on marginal gyrus. In 7 experiments on the marginal gyrus (29%), no increase in Kp greater than 1 mM occurred. In contrast, EEG amplitude on this gyrus was reduced by middle cerebral artery occlusion in 25 of 26 experiments, and it is concluded that this gyrus is the principal site of ischaemic penumbra in the model; in 41% of experiments similar conditions were also present on the suprasylvian gyrus.

Animals↗

The cortical ischaemic penumbra associated with occlusion of the middle cerebral artery in the cat: 2. Studies of histopathology, water content, and in vitro neurotransmitter uptake.

The nature of the ischaemic penumbra, as defined by suppression of electroencephalogram amplitude in the absence of increase in steady state pial surface potassium activity in excess of 13 mM, was examined in the marginal gyrus of cats subjected to middle cerebral artery occlusion. In vitro synaptosomal neurotransmitter uptake, water content (specific gravity), and histopathology at the light and electron microscopic level were studied and the results compared with those obtained at deeper, critical levels of ischaemia (less than 15 ml 100 g-1 min-1). [3H]4-Aminobutyric acid uptake was 104% of control in the marginal gyrus (NS), and 61 and 48% (p less than 0.05) in critical ischaemia. It is concluded that impairment of in vivo synaptosomal uptake is a marker of simultaneous widespread damage to neurones, rather than of a change restricted to the synaptic compartment, although the present findings cannot exclude reversible, substrate-limited impairment of uptake in vivo. Reductions in specific gravity were seen only with critical ischaemia. In 5 of 6 experiments, early or classical ischaemic neuronal cell changes and reactive glia were seen on light microscopy in restricted areas in the marginal gyrus, either in microfoci or scattered more diffusely. Ultrastructural changes were more frequent but were considered to affect only a minority of neurones. Hypotheses for selective electrophysiological suppression in penumbra are discussed.

Animals↗

Brain abscess.

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Adrenal Cortex Hormones↗

Kinetics of resolution of transient increases in extracellular potassium activity: relationships to regional blood flow in primate cerebral cortex.

Previous studies have established that in cerebral cortex subjected to progressive reduction in blood flow, two distinct thresholds of flow may be identified below which cellular function is impaired: the cortical evoked response loses amplitude when local flow falls below 18ml/100gm/min, and below 11ml/100gm/min a major increase in extracellular K+ activity (Ke) occurs. However, further evidence suggests that even at higher flows the capacity of the tissue to handle induced ionic changes may be impaired. To investigate this point, we studied the kinetics of resolution of Ke following a transient increase produced by local electrical stimulation, in relation to the local pre-stimulus flow (reduced by acute middle cerebral artery occlusion) in baboons. Flow was measured by the hydrogen clearance method and Ke by ion-exchanger micro-electrodes, in the same cortical regions. In primary induced transients (those increases in Ke elicited by cortical stimulation, and reported previously,) Ke attained a maximum value of 8-10 mM and then decayed towards the 4-mM baseline. The half-time of this decay was significantly increased from normal in the flow range 20-40 ml/100 gm/min, and increased further at lower flows until, below 11ml/100gm/min, Ke clearance was undetectable. Thus, cortical ion homeostasis appeared impaired at flows substantially closer to normal than those thresholds mentioned above, a result discussed in terms of impairment of active Ke clearance mechanisms. Secondary induced transients arose during a primary induced transient, reaching considerably higher peak values (8-30 mM) of Ke (indicating temporary clearance loss) and with slower decay rate than the primary. Spontaneous transients, not associated with any stimulus, were also observed; like secondary transients, they occurred only at flows below 20ml/100gm/min and showed a reduction in clearance rate with progressive ischemia. They resemble spreading depression and their generation is discussed in terms of the ionic and metabolic conditions at their time of origin.

Animals↗

Synaptosomes prepared from fresh human cerebral cortex; morphology, respiration and release of transmitter amino acids.

Synaptosomes prepared from fresh human cerebral cortex were shown to be morphologically similar to those from other species. On incubation, they took up oxygen at a high and linear rate and accumulated potassium against a concentration gradient. In response to depolarization by raised extracellular K+ or addition of veratrine, they showed increased respiration, lowered tissue potassium, and enhanced release of glutamate, aspartate and GABA. The preparation may be of value for studies of neurological disorders.

Amino Acids↗

Fifteen-year review of the mortality of brain abscess.

Ninety consecutive cases of brain abscess admitted to this center between 1964 and 1978 have been reviewed. The overall mortality has fallen in three consecutive 5-year periods from 42 to 21 to 9.7%. A number of factors seem to be responsible for this. Early surgical intervention was associated with the reduction in mortality between the first and second 5-year periods. Recognition of the significance and extent of cerebral edema, confirmed since computed tomographic (CT) scans have been available, led to a greater use of steroids during the last 5-year period, but the number of patients thus treated was too small to permit an assessment of any effect on mortality. There is no evidence to suggest a change in the natural history of the disease, and surgical management has not altered significantly. Experience with CT scanning in this center in the diagnosis of brain abscess is limited. It is therefore not possible no assess whether any improvement in mortality may have arisen from the early and accurate diagnosis obtainable with this technique. Improvement in culture technique has been of major importance, leading to a better understanding of the bacteriology of brain abscesses. This has allowed a more rational antibiotic program to be instituted, in particular the use of agents active against obligate anaerobes.

Anti-Bacterial Agents↗

Reversibility of ischaemically induced changes in extracellular potassium in primate cortex.

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.

Animals↗

Extracellular potassium activity, evoked potential and tissue blood flow. Relationships during progressive ischaemia in baboon cerebral cortex.

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).

Animals↗