Abstract
Although the exact pathophysiology of critical illness polyneuropathy (CIP) is still
unknown, there are several hypotheses, some of which are increased inflammation and
oxidative stress. We used rodent sepsis model in which we induced sepsis through cecal
ligation followed by cecal puncture. We then administered ascorbic acid (AA) and evaluated
outcomes. The levels of malondialdehyde (MDA), tumor necrosis factor α (TNF-α), interleukins
(IL)-6 in the plasma, and heat shock protein-70 (HSP-70) levels in the sciatic nerve
were measured, and also electromyography analyses were performed. While plasma MDA,
TNF-α, and IL-6 levels were decreased significantly with AA treatment, sciatic nerve
levels of HSP-70 were significantly elevated in the AA group. A significant increase
in compound muscle action potential (CMAP) amplitude and a significant decrease in
CMAP latency were detected in the AA group. We observed healing effects of AA on a
rat model of CIP and these effects seem to be related to its anti-inflammatory and
antioxidant properties.
Keywords
critical illness polyneuropathy - sepsis - ascorbic acid - malondialdehyde - compound
muscle action potential
