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Biomedical subjects

N M Branston

Publications and source records attributed to N M Branston.

At least 55 records · Page 3Linked to original sources
PubMed1976

The effect of intracranial hypertension on cerebrovascular resistance--an experimental study.

Pulse transmission through cortex between a vein and artery in the middle cerebral distribution has been used as an index of vascular resistance in the middle cerebral field in baboons. Following catheterisation of these small vessels, the skull has been reconstituted and the effect of intracranial hypertension produced by cisternal infusion has been studied. An earlier linear relaxation of resistance in relation to rising intracranial pressure has been succeeded by a second phase in which pulse transmission increases quite profoundly despite minimal further increase in intracranial pressure. This appears to represent the exhaustion of the compliance of the vascular compartment, and corresponds closely to levels of intracranial pressure at which failure of autoregulation to increased intracranial pressure has been observed in previous experiments. Spontaneous bursts of transient increased pressure made their appearance in a number of animals at this level of pressure. The possible significance of increased pulse transmission following exhaustion of compliance in relation to breakdown of the blood brain barrier and potential spreading oedema is discussed.

Animals↗
PubMed1976

Measurements of oxygen tension in the cerebral cortex of baboons.

A polystyrene-covered platinum electrode (100-150 mum diameter) has been used to measure cortical tissue oxygen tension in baboon brains. The method of preparation, calibration, and the importance of small residual current (less than 40 nA) as an attribute of a reliable electrode, are described. With electrodes of this size, there was a large (16 +/- 12nA/torr) and linear current output with pO2 changes. The effect of avrious gases in addition to oxygen is described; halothane inhalation increases the apparent pO2 and hydrogen, used for blood flow estimations, reduces the recorded pO2. In 48 separate electrode placements in 13 baboons, the mean cortical qo2 was 23.8 +/- 12 mm Hg, with a range from 1-79 mm Hg; following occlusion of one middle cerebral artery, 37 electrodes recorded a pO2 of less then 5 mm Hg pO2 Oscillations were invariably noted in control conditions, independent of blood pressure; these waves disappeared during MCA occlusion and appeared to be augmented following release of the clip. Blood pressure "spikes" produce immediate and synchronous changes in all electrodes entirely different from the spontaneous waves. Such blood pressure changes may mask the true effect of hypercapnia on tissue pO2 and, if ignored, may lead to erroneous assumptions regarding local neural control of the circulation, the increased pO2 secondary to hypertension being regarded as evidence of regional vasodilation. A SUdden change in inspired pO2-the "air test"-was performed in control conditions and following the ischaemic insult, and the rate of change of cortical pO2 compared. The gradient was significantly greater (P less than 0.05) following ischaemia, suggesting a changed ratio in the tissue's flow to oxygen requirements and/or a persisting vasodilatation.

Animals↗
PubMed1976

Changes in regional cortical tissue oxygen tension and cerebral blood flow during temporary middle cerebral artery occlusion in baboons.

Cortical tissue oxygen measured by a platinum cathode, and cerebral blood flow recorded by a hydrogen clearance technique, were measured in 13 baboons before, during and after temporary occlusion of the middle cerebral artery. Mean control pO2 was 23.8 +/- 14 mm Hg and mean flow 51.3 +/- 12 ml/100g/min. During the occlusion, there was a gradation in pO2 from values in the opercular area of 3.6 +/- 5.9 mm Hg, to values in the high parietal area of 11.9 +/- 11.7, these being statistically different (P less than 0.05) from each other. The corresponding flow values were 5.5 +/- 7.5 (opercular) and 22.3 +/- 21.7 ml/100 g/min parietal (P less than 0.01). Following removal of the MCA clip, between 20% and 30% of the electrodes registered an early hyperoxia and hyperaemia, which lasted up to 5 min. A late and prolonged hyperoxia, with less evidence of hyperaemia, was also noted in about 20%. The mean tissue pO2, however, at 5-min intervals up to 40 min following the removal of the clip only reached 60-80% of control values in the most ischaemic areas. Only the parietal region showed a mean pO2 above control levels. The mean flow data were uniformly reduced in all regions to about 80% of control values. During and after a second occlusion in 6 animals, similar changes were noted but with even fewer instances of hyperoxia. The mean oxygen and flow results were lower than with the first occlusion, but the reduction was not significant. There was no overall effect of hypercapnia on cortical tissue pO2 during the control period, but there was a significant (P less than 0.05) reduction during the same procedure after the period of ischaemia. An increase in pO2 during hypercapnia could be observed if there were arousal responses of blood pressure "spikes".

Animals↗
PubMed1974

Effect of supratentorial space-occupying lesions on regional intracranial pressure and local cerebral blood flow: an experimental study in baboons.

Cortical blood flow and epidural intracranial pressure have been measured in the two supratentorial compartments of the intracranial space in experimental baboons during the acute expansion of a parieto-occipital epidural balloon. Differential pressures between the two halves of the supratentorial space have been found, and these have been associated with evidence that flow has fallen more quickly in the hemisphere most compressed. The evidence points to a more rapid exhaustion of the autoregulatory capacity in the hemisphere subjected to greater compression, a fall in perfusion pressure to below critical autoregulatory levels occurring slightly before that in the opposite hemisphere, and the establishment of a differential flow pattern for a short time during a critical phase of compression. The displacements induced by inflation of the parieto-occipital balloon have been described.

Animals↗
PubMedDate not supplied

Changes in somatosensory evoked potentials following an experimental focal ischaemic lesion in thalamus.

Experiments have been performed to produce localized thalamic ischaemia in baboons anaesthetised with alpha-chloralose. Somatosensory evoked potentials to median nerve stimulation were recorded in the medial lemniscus, VPL of thalamus and the primary somatosensory cortex. Local blood flow was also recorded by the hydrogen clearance technique in these regions. The early potential recorded in thalamus has been shown to be generated from 3 sources: (i) a positivity generated outside the VPL, (ii) local wavelets, most likely from synaptic activity close to the recording electrode, and (iii) a local overall negativity. The first of these potentials alone remains after thalamic ischaemia. It arises below the level of the thalamus, being very likely generated by the afferent volley in the medial lemniscus, and is seen in the surface-recorded response as the early component P8 (corresponding to P15 in the human).

Animals↗
PubMedDate not supplied

The effect of experimental ischaemia on the direct cortical response of the motor cortex in primates.

We studied the changes in amplitude of the first short latency positive potential (2.3 +/- 0.3 msec, mean +/- S.D.) of the direct cortical response (DCR) elicited by surface electrical stimulation of the motor cortex in anaesthetised baboons. Local cortical blood flow, measured by the hydrogen clearance method, was progressively reduced by acute middle cerebral artery occlusion and subsequent hypotension and was related to the amplitude of this potential. With flow levels greater than 25 ml/100 g/min the DCR was essentially unaffected, but it was lost with flows below 20 ml/100 g/min. These results indicate a threshold relationship between the generation of the electrical activity evoked in the cortical elements and local cortical flow, similar to that previously demonstrated for cortical somatosensory evoked potentials.

Animals↗
PubMedDate not supplied

Early components of transcallosal responses in acute ischaemia of the corpus callosum.

In 8 baboons maintained under propofol anaesthesia, transcallosal evoked responses were recorded from the primary motor cortex following electrical stimulation of the contralateral homotopic cortical surface. The corpus callosum was made ischaemic by transorbital occlusion of the common anterior cerebral artery; blood flow (measured by the hydrogen clearance method) in the stimulating and recording regions was not significantly affected by this procedure. The transcallosal responses from the normally perfused brain contained early positive (P1) and negative (N1) components. As stepwise ischaemia was produced in the corpus callosum, the amplitude of P1 initially increased up to 150% of control and the peak latency of P1 was significantly prolonged. At flows below 8 ml/100 g/min the amplitude rapidly decreased. Wave form changes and flow threshold of N1 were similar to those of P1. These results suggest that measurement of early transcallosal responses could be useful clinically as monitors of the ischaemic level in anterior cerebral artery territory.

Acute Disease↗
PubMedDate not supplied

Ischemic brain edema following middle cerebral artery occlusion in baboons: relationship between regional cerebral water content and blood flow at 1 to 2 hours.

The relationship between increase in water content in ischemic brain and levels of regional blood flow has been studied in 11 primates. Flows were recorded using the method of hydrogen (2-minute) clearance, from a total of 128 electrodes in cortex and white matter, and a gradation of ischemia was produced by middle cerebral occlusion transorbitally. The flows were reduced in the area of densest ischemia from control levels of 12.0 +/- 12.0 ml/100g/min to 7.0 +/- 5.4 ml/100g/min, with lesser decreases over the remainder of the ischemic hemisphere. Water content was measured in cortex and white matter, in regions topographically related to those of flow measurements, by densitometric assessment using precalibrated kerosene/bromobenzine columns. The average water content of cortex in regions remote from ischemia was 797.4 +/- 5.8 mg/gm and in white matter 708.5 +/- 8.2 mg/gm. Significant increases in water content (comparing corresponding regions of the two hemispheres) of up to 11.4 +/- 7.5 mg/gm were demonstrated in the most ischemic cortical areas. A gradient of water increase was evident in the ischemic hemisphere, increases water content being greatest in the opercular zone and least in the parasagittal area. Significant differences in white matter water content between the 2 hemispheres were demonstrated only in the most densely ischemic areas in the current experiments where ischemia was limited to 93 +/- 20 mins in the 11 animals without reperfusion. The relationship between ischemic density and water content increase showed that significant increases in water content occurred in regions where terminal flows had been below 20 ml/100g/min, indicating that accumulation of water in ischemic brain begins at flow values comparable to those associated with the failure of synaptic transmission, higher than those associated with failure of the ionic pump of the cell. Possible pathophysiological mechanisms are discussed.

Animals↗
PubMedDate not supplied

Central conduction time in primate brain ischemia -- a study in baboons.

The relationship between central conduction time (CCT) and levels of regional blood flow were studied in 9 primates. Flows were recorded in both hemispheres using the method of hydrogen (2 min) clearance. The somatosensory evoked potentials were recorded over the contralateral cortex and the dorsal columns, following median nerve stimulation. The CCT, a measure of the brain's electrical conduction, was determined by the difference in latencies between N10, (the arrival of the afferent volley at the sensory cortex) and N7 (its arrival at the dorsal column). Ischemia was produced by transorbital occlusion of the right middle cerebral artery. In the acute ischemic phase within 5 minute of occlusion, there was a significant correlation between the change in CCT and the decrease in flow. In the later occlusive phase, the CCT was unaltered with flows above 15 ml/100g/min. Below that level smaller decreases in flow resulted in progressively larger changes in CCT until a flow was reached where the N10 disappeared or the entire cortex was electrically silent. Focal ischemia had no effect on the first positive deflection recorded from the cortex (P8) or the first negative peak response from the cervical region (N7). However, the latency of P8 was increased or it was absent with the introduction of hypotension, while N8 was unaltered. From our measurements, it appears that prolongation of CCT can be related to developing ischemia, and that the thresholds for change are not dissimilar to those already recorded for somatosensory evoked responses to the basis of amplitude alterations in the cortex. Below these levels, prolongation of CCT appears to bear a parametric relationship to alteration in blood flow. While the measurement displays only one of the many alterations which are induced by ischemia in the brain, its attraction lies in its simplicity and in the fact that it may be applied with relative ease in the clinical situation. Under these circumstances, it appears to be an adequately sensitive monitor of developing brain ischemia, and deserves further study.

Acute Disease↗