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O A Peiris

Publications and source records attributed to O A Peiris.

13 recordsLinked to original sources
PubMed1972

Effects of hyperkalaemia on the excitability of peripheral nerve.

An experimental animal model has been developed for the study of excitability change in peripheral nerve during limb ischaemia. This model has been used to investigate the effects of hyperkalaemia on the sequence of excitability change that occurs during cuff-induced limb ischaemia and in the post-ischaemic recovery period. The results lend support to the hypothesis that the dynamics of K ion concentration in the periaxonal space play a critical role in determining these excitability changes and that the polyanionic mucopolysaccharide gap substance of the node of Ranvier is likely to constitute the diffusion barrier that defines the periaxonal space.

Action Potentials↗
PubMed1970

The role of diffusion barriers in determining the excitability of peripheral nerve.

The excitability changes occurring in normal isolated peripheral nerves of rats have been studied during exposure to hypoxic and anoxic conditions before and after the administration of insulin. The changes observed have been explained in terms of the dynamics of K' equilibrium in the periaxonal spaces, and attention is drawn to the importance of the relative impermeability of the periaxonal diffusion barrier in determining this equilibrium. Isolated peripheral nerves from alloxan-diabetic rats, studied under similar conditions, show significant differences in the sequence of their excitability changes. It has been shown that the rate of change of excitability in these nerves is slower than those of control nerves. These results have now been interpreted in terms of the K' changes in the periaxonal space. It is concluded that these slower excitability changes are due to an increase in the permeability of the diffusion barrier of the diabetic nerve to potassium.

Animals↗
PubMed1970

Peripheral nerve function in chronic liver disease.

Peripheral nerve function has been studied in 50 patients with chronic liver disease. An increase in the latency or a reduction in the response amplitude of the evoked sensory potential of the median nerve was detected in 34 of the 50 subjects. This was in striking contrast to the paucity of neurological signs and symptoms suggestive of peripheral nerve damage seen in these patients. There was no evidence to show that alcohol was responsible for the neuropathy. Abnormalities in the excitability changes of sensory nerve during ischaemia were detected in seven of the 16 subjects whose distal sensory latencies were within normal limits. A critical evaluation of the hypotheses which have been postulated to account for the increased resistance of peripheral nerve to inactivation by ischaemia has been made. It is concluded that an increase of the permeability of the periaxonal diffusion barrier to K offers the most acceptable explanation for this phenomenon.

Adult↗