Published in:
Open Access 01-02-2007 | Research
Neuromuscular deterioration in the early stage of sepsis in rats
Published in: Critical Care | Issue 1/2007
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Introduction
Critical illness polyneuropathy (CIP) is a clinical condition frequently seen in patients being treated in critical care units in the final stage of sepsis. The etiopathology of CIP is still unclear, and the onset time of appearance of the electrophysiological findings has not been elucidated. The very little research that has been carried out on this topic is limited to clinical electrophysiological and histopathological studies. In this study, electrophysiological alterations in the early stage of experimentally induced sepsis were investigated in septic rats.
Methods
We conducted a prospective, randomized, controlled experimental study in an animal basic science laboratory with 30 male Sprague-Dawley rats, weighing 200 to 250 g. All of the rats were randomly assigned to one of two groups. In the sepsis group (n = 20), cecal ligation and puncture (CLP) was performed to induce experimental sepsis. In the sham-operated group (n = 10), laparotomy without CLP was performed. Before and 24 hours after CLP and laparotomy, the right sciatic nerve was stimulated from the sciatic notch and compound muscle action potentials (CMAPs) were recorded from the gastrocnemius muscle. Recordings of latency, amplitude, and duration of the CMAP were evaluated.
Results
CMAP durations before and 24 hours after surgery were 0.45 ± 0.05 ms and 0.48 ± 0.05 ms, respectively, in the sham-operated group and 0.46 ± 0.05 ms and 0.55 ± 0.01 ms, respectively, in the sepsis group. Latency measurements in the sham-operated group were 0.078 ± 0.010 ms and 0.080 ± 0.015 ms, respectively, whereas measurements were found to be prolonged in the sepsis group: 0.094 ± 0.015 ms and 0.149 ± 0.054 ms before and 24 hours after surgery, respectively (p < 0.05). CMAP amplitudes in the sham-operated group before and 24 hours after surgery were 8.41 ± 0.79 mV and 8.28 ± 1.92 mV, respectively, whereas in the sepsis group the amplitude measurements decreased to 7.60 ± 1.75 mV and 4.87 ± 3.44 mV, respectively (p < 0.05).
Conclusion
The results of the study indicate that electrophysiological alterations appear in the first 24 hours after experimental sepsis and are characterized by an increase in latency and a decrease in CMAP amplitude. The results also suggest that electrophysiological findings seen in patients with CIP might appear before clinical signs of CIP.