Is resistance to ischaemia of motor axons in diabetic subjects due to membrane depolarization?

The reasons for the resistance to ischaemia of peripheral nerves in
diabetics are not well understood. We have now explored whether
axonal depolarization underlies this phenomenon, as has previously
been proposed. Resistance to ischaemia was determined by the new
method of “threshold tracking”. This method revealed an increase in
excitability of the peroneal nerve at the popliteal fossa during
ischaemia, and a decrease in excitability in the post-ischaemic
period. The extent of these alterations in 28 type 1 diabetics
without peripheral neuropathy showed a strong correlation with the
mean blood glucose concentrations during the last 24 h before
examination. To test whether the ischaemic resistance was related
to membrane potential, we also measured axonal superexcitability in
11 selected diabetics, since it has been shown that post-spike
changes in excitability depend on membrane potential. Changes in
excitability of the peroneal nerve were measured in the period
between 10 and 30 msec following a conditioning supramaximal
compound action potential. Under resting conditions, no differences
in the post-spike superexcitability were found between controls and
diabetics, despite striking differences in their responses to a
10-min pressure cuff. These observations indicate that membrane
depolarization is not involved in the resistance to ischaemia of
motor axons in diabetic subjects.