<p>Sensory-selective nerve blockade is highly useful for pain management in clinical practice, but developing such blockers remains challenging. A major handicap is the lack of objective in vivo animal models to evaluate motor and sensory nerve conduction simultaneously. Due to anatomical structures, motor evoked potentials (MEPs) and/or somatosensory evoked potentials (SSEPs) may be used to assess nerve conduction. MEPs were elicited by stimulating motor cortex and recorded from contralateral hind limb. SSEPs were generated by stimulating sciatic nerve and recorded from contralateral sensory cortex. Amplitude/latency changes were recorded under various physiological conditions (e.g., anesthesia, durations, temperatures, and oxygen) and drug interventions for validation. Compared to sevoflurane, propofol minimally inhibited MEPs at sedative doses and was therefore used during recordings. Both hypothermia (34–36 °C) and hyperthermia (38–40 °C) significantly suppressed MEP and SSEP amplitudes (<i>P</i> &lt; 0.0001). Reduced oxygen saturation (SaO<sub>2</sub>) decreased MEP amplitudes (<i>P</i> &lt; 0.0001), and the amplitudes were strongly correlated with SaO<sub>2</sub> (R<sup>2</sup> = 0.8284). For selective blockade validation, lidocaine suppressed both MEP and SSEP amplitudes below 20% of baseline (<i>P</i> &lt; 0.0001), confirming non-selectivity. In contrast, QX-314/capsaicin selectively suppressed SSEPs (<i>P</i> &lt; 0.0001), while MEPs remained stable. This model is stable for evaluating selective nerve blockade in vivo for at least 60&#xa0;min under controlled physiological conditions.</p>

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An in vivo rat model for comparing selective blockade between sensory and motor nerve conduction

  • Yi Teng,
  • Xian Zou,
  • Jin Liu,
  • Xiangyu Hu,
  • Cheng Zhou,
  • Mengchan Ou

摘要

Sensory-selective nerve blockade is highly useful for pain management in clinical practice, but developing such blockers remains challenging. A major handicap is the lack of objective in vivo animal models to evaluate motor and sensory nerve conduction simultaneously. Due to anatomical structures, motor evoked potentials (MEPs) and/or somatosensory evoked potentials (SSEPs) may be used to assess nerve conduction. MEPs were elicited by stimulating motor cortex and recorded from contralateral hind limb. SSEPs were generated by stimulating sciatic nerve and recorded from contralateral sensory cortex. Amplitude/latency changes were recorded under various physiological conditions (e.g., anesthesia, durations, temperatures, and oxygen) and drug interventions for validation. Compared to sevoflurane, propofol minimally inhibited MEPs at sedative doses and was therefore used during recordings. Both hypothermia (34–36 °C) and hyperthermia (38–40 °C) significantly suppressed MEP and SSEP amplitudes (P < 0.0001). Reduced oxygen saturation (SaO2) decreased MEP amplitudes (P < 0.0001), and the amplitudes were strongly correlated with SaO2 (R2 = 0.8284). For selective blockade validation, lidocaine suppressed both MEP and SSEP amplitudes below 20% of baseline (P < 0.0001), confirming non-selectivity. In contrast, QX-314/capsaicin selectively suppressed SSEPs (P < 0.0001), while MEPs remained stable. This model is stable for evaluating selective nerve blockade in vivo for at least 60 min under controlled physiological conditions.