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N M Branston

Publications and source records attributed to N M Branston.

64 records · Page 4Linked to original sources
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Modulation of the pathophysiology of primate focal cerebral ischaemia by indomethacin.

The effect of indomethacin (3mg/kg IA) preloading on the pathophysiology of a model of acute cerebral ischaemia has been tested. Primates anaesthetised with alpha-chloralose were used. Indomethacin reduced basal blood flow by 39% and reduced CO2 reactivity by 71%. Water content changes of the cerebral cortex and relationships between blood flow and extracellular potassium (Ke), and calcium (Cae) activities have been measured. Indomethacin infusion did not effect the water content of the left side but there was more water in all regions of the right hemisphere which were rendered ischaemic. There water increases were significant for blood flows greater than 5ml/100g/min in exposed areas. There was a significant increase in the flow thresholds for change in Ke and Cae. Possible mechanisms for these changes have been discussed.

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The effects of a calcium antagonist, nimodipine, upon physiological responses of the cerebral vasculature and its possible influence upon focal cerebral ischaemia.

The effects of a calcium antagonist, nimodipine, were tested on the response of the cerebral circulation to arterial pCO2 and blood pressure changes. The effects of reduced blood flow upon oedema formation and extracellular ion homeostasis under nimodipine preloading were studied. Both open and closed skull primate models were used, with alpha-chloralose anaesthesia. Nimodipine infusion increased basal blood flow in the open skull, but not the closed skull animals. Autoregulation to increased blood pressure was little affected. Responses to arterial pCO2 changes and autorerulation to reduced blood pressure were severely imparied. Residual blood flow after middle cerebral artery occlusion was significantly higher with nimodipine than in controls. The threshold levels of blood flow for the development of cortical oedema and for disturbance of ion homeostasis were, however, increased, suggesting that nimodipine interferes with cellular energy metabolism and increases the susceptibility of tissue to ischaemic damage.

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A model of selective experimental ischaemia in the primate thalamus.

A model for studying changes in local CBF and evoked potentials in selective thalamic ischaemia has been developed. The arterial supply to the posterior thalamus (mainly from the posterior choroidal arteries) was occluded in the baboon using a transorbital approach to the region of prepontine and ambient cisterns. Local CBF was measured by the hydrogen clearance method using electrodes introduced into the nucleus ventralis posterior lateralis of thalamus as well as cortex on both sides. The production of focal ischaemia was demonstrated by a significant decrease in thalamic CBF and confirmed by examination of the brain perfused with carbon particles.

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Local cerebral blood flow and vascular reactivity in a chronic stable stroke in baboons.

Blood flow in the hemispheres of baboons three years after middle cerebral artery occlusion has been assessed by the hydrogen clearance technique. Blood flow in the infarct itself varied from very low (8 ml/100 gm per minute) to very high (89 ml/100 gm per minute) values and, averaging the values for the infarct as a whole, it was impossible to distinguish average flows in the infarct from those of the normal hemisphere. Flow values in surrounding zones of the infarct remained significantly lower than those of comparable normal hemispheres, and, excluding the infarct, the mean average hemispheral blood flow was 35.2 ml/100 gm per minute. This indicates a significant reduction in flow in the cortex, subsequently shown histologically to be normal, compared with normal blood flow values for the baboon hemisphere. Autoregulation was lost in the infarct and impaired in surrounding tissue. CO2 reactivity was grossly reduced in the hemisphere as a whole but was present in all areas, even occasionally in electrode placements within the infarct itself. After perfusion fixation of the head, pathological study of the area of infarction showed a fairly consistent distribution, the infarct itself consisting of many dilated blood vessels of non-capillary nature scattered among fibrous tissue in what was virtually a glial scar.

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Recovery of the cortical evoked response following temporary middle cerebral artery occlusion in baboons: relation to local blood flow and PO2.

The degree of recovery of the somatosensory cortical evoked response following a period (15 to 65 minutes) of partial ischemia, produced by temporary occlusion of the middle cerebral artery (MCA), was assessed in baboons and related to the local tissue blood flow and PO2 before, during and after the occlusion. Flow was measured using the technique of two-minute hydrogen clearance. Failure of complete recovery of the evoked response was associated with significantly greater depths of ischemia and tissue hypoxia during occlusion, and with significantly greater and persisting tissue hypoxia after occlusion, than complete recovery. Complete recovery of the evoked response also was associated with tissue hyperoxia after occlusion. The reduced postocclusive PO2 levels associated with incomplete recovery of the evoked response suggest that reduced perfusion during ischemia was sufficiently severe to cause some degree of irreversible anoxic damage. The effect of a brief (three to ten minutes) period of ventilation with air (instead of oxygen) under such low-flow conditions was to depress the evoked response significantly further; normally perfused brain, however, was unaffected by this procedure. This finding has clinical implications in regard to normobaric oxygen therapy.

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Autoregulation in acute focal ischemia. An experimental study.

The autoregulatory capacity of areas of the cerebral circulation subjected to ischemia by acute middle cerebral occlusion has been assessed in experimental primates. Autoregulation was tested to a rise in blood pressure induced by aramine, and to a fall in blood pressure induced by exsanguination. Whole hemisphere autoregulation was substantially disturbed due to both increased blood pressure and lowered blood pressure, but fractionation of this response indicated that autoregulation to increased blood pressure was preserved in the parasagittal and intermediate zones of the hemisphere, and totally lost in the region of the sylvian opercula where middle cerebral occlusion had produced the most dense ischemia. In relation to reduced perfusion pressure, autoregulation was again widely impaired and assessment of the degree of impairment by areas indicated no significant difference between the areas of the sylvian opercula and the remainder of the lateral aspect of the hemisphere studied. Where the degree of ischemia in each individual electrode was assessed, however, it appeared that the degree of auto-regulatory loss to decreased perfusion pressure was dependent upon the intensity of ischemia, and autoregulation was partially preserved in electrodes whose immediate post-occulsion flow values were greater than 40% of basal flow. Retransfusion following exsanguination in animals with acute middle cerebral occlusion indicated that there was a linear relationship between the degreee of reperfusion achieved by retransfusion and the intensity of ischemia induced by exsanguination following middle cerebral occlusion. Thus there was some support for the no-reflow phenomenon in intensely ischemic areas.

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Cortical evoked potential and extracellular K+ and H+ at critical levels of brain ischemia.

As shown previously, the electrical function of the brain is critically dependent on cerebral blood flow in the sense that reduction beyond an ischemic threshold of approximately 15 ml/100 gm per minute (approximately 35% of control) in the baboon leads to complete failure of the somatosensory evoked response. This study tests the hypothesis that electrical failure in ischemia may be directly associated with a massive release of intracellular K+ or with a critical degree of extracellular acidosis. By microelectrode techniques, measurements of blood flow, extracellular activity of K+ and H+ as well as evoked potential were made in the baboon neocortex. Reductions in blood flow were obtained by occlusion of the middle cerebral artery and depression beyond the ischemic threshold of electrical function achieved by a reduction of systemic blood pressure which, in the ischemic zones, changed local cerebral blood flow proportionally. Abolition of evoked response could not be explained by depolarization by release of intracellular K+, nor was it critically dependent on cortical pH. However, the massive release of intracellular K+ was by itself critically dependent on cortical blood flow and occurred at 18 greater than 6 greater than 2 ml/100 gm per minute (median with 5% confidence limits). Thus a dual threshold in ischemia for neuronal function is described, the threshold for release of K+ being clearly lower than the threshold for complete electrical failure. Further, the findings support the concept of an ischemic penumbra during which the neurons remain structurally intact but functionally inactive. That neurons can survive for some time in this state of lethargy is evidenced by the observations that an increase in rCBF, if sufficient, can restore evoked potential and normalize extracellular K+ activity as well as pH.

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