<p>This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</p> <p>Diabetes mellitus produces marked abnormalities in
motor nerve conduction, but the mechanism is not
clear. In the present study we hypothesized that in
the streptozotocin (STZ)-induced diabetic rat impaired
vasodilator function in arterioles that provide
circulation to the region of the sciatic nerve is
associated with reduced endoneural blood flow
(EBF) and that these defects precede slowing of
motor nerve conduction velocity, and thereby may
contribute to nerve dysfunction. As early as three
days after the induction of diabetes endoneural
blood flow was reduced in the STZ-induced diabetic
rat. Furthermore, after 1 week of diabetes acetylcholine-
induced vasodilation was found to be impaired.
This was accompanied by an increase in the superoxide
level in arterioles that provide circulation to
the region of the sciatic nerve as well as changes in
the level of other markers of oxidative stress
including an increase in serum levels of thiobarbituric
acid reactive substances and a decrease in lens
glutathione level. In contrast to the vascular related
changes that occur within 1 week of diabetes, motor
nerve conduction velocity and sciatic nerve Na<sup>+</sup>/k<sup>+</sup>
ATPase activity were significantly reduced following
2 and 4 weeks of diabetes, respectively.
 These studies demonstrate that changes in vascular function
in the STZ-induced diabetic rat precede the
slowing of motor nerve conduction velocity (MNCV)
and are accompanied by an increase in superoxide
levels in arterioles that provide circulation to the
region of the sciatic nerve.</p>
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Int J Exp Diabetes Res. 2000; 1(2):131-143