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Sepsis induces early phrenic nerve neuropathy in rats
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The aim of the present study was to investigate the electrophysiology of the phrenic nerve and the diaphragm muscle during sepsis.In total, 26 rats underwent either sham laparotomy or caecal ligation and puncture (CLP). Electrophysiology was evaluatedviaa phrenic nerve conduction study and needle electromyography of the diaphragm, prior to CLP, 6 and 24 h post-CLP and on day 7. The histopathology of the diaphragm muscle and phrenic nerve was also examined on day 7.In the sepsis group, the phrenic nerve conduction study showed decreased amplitude of compound action potential (CMAP), and prolongation in the duration and the latency of CMAP. The diaphragmatic needle electromyography showed decreased amplitude and frequency of the motor unit action potential (MUP), and prolongation in the duration of MUP, at all time points, compared with the pre-CLP values. The electrophysiological abnormalities were consistent with axonal and demyelinating phrenic nerve neuropathy. Electrophysiological abnormalities were present at 6 h with worsening at 24 h and on day 7. Histopathological examination showed normal muscular fibres and focally slight myelin degenerations of the phrenic nerve fibres.In conclusion, sepsis induced phrenic nerve neuropathy as early as the 6th h in rats.
European Respiratory Society (ERS)
Title: Sepsis induces early phrenic nerve neuropathy in rats
Description:
The aim of the present study was to investigate the electrophysiology of the phrenic nerve and the diaphragm muscle during sepsis.
In total, 26 rats underwent either sham laparotomy or caecal ligation and puncture (CLP).
Electrophysiology was evaluatedviaa phrenic nerve conduction study and needle electromyography of the diaphragm, prior to CLP, 6 and 24 h post-CLP and on day 7.
The histopathology of the diaphragm muscle and phrenic nerve was also examined on day 7.
In the sepsis group, the phrenic nerve conduction study showed decreased amplitude of compound action potential (CMAP), and prolongation in the duration and the latency of CMAP.
The diaphragmatic needle electromyography showed decreased amplitude and frequency of the motor unit action potential (MUP), and prolongation in the duration of MUP, at all time points, compared with the pre-CLP values.
The electrophysiological abnormalities were consistent with axonal and demyelinating phrenic nerve neuropathy.
Electrophysiological abnormalities were present at 6 h with worsening at 24 h and on day 7.
Histopathological examination showed normal muscular fibres and focally slight myelin degenerations of the phrenic nerve fibres.
In conclusion, sepsis induced phrenic nerve neuropathy as early as the 6th h in rats.
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