Journal of anesthesia · 2025
Effects of hemorrhage, fluid resuscitation, and transient deep anesthesia on transcranial and transesophageal motor evoked potentials in a swine model.
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Kurita Tadayoshi, Kawashima Shingo, Khaleelullah Mohamed Mathar Sahib Ibrahim, Nakajima Yoshiki
Аннотация
PURPOSE: Hemorrhage may suppress the amplitude of transcranial motor evoked potentials (TcMEPs). We compared the effects of hemorrhage, subsequent fluid resuscitation, and transient anesthetic deepening on the recently developed transesophageal motor evoked potentials (TeMEPs) with those on conventional TcMEPs.
METHODS: Twelve swine (26.0 ± 0.5 kg) were anesthetized with 8-13% desflurane during preparation and then switched to propofol and remifentanil anesthesia. After baseline measurements, 700 mL of blood was withdrawn over 30 min to induce hypovolemia. Hypovolemia was then treated with 700 mL of hydroxyethyl starch for 30 min (fluid resuscitation). Subsequently, 5 mg of remimazolam was administered, followed by 50 mg of propofol after the effects of remimazolam had reversed. TcMEPs and TeMEPs were recorded at the end of each condition and immediately before and after the administration of remimazolam or propofol.
RESULTS: In all conditions and in all limbs, TeMEPs' amplitudes were greater than those of TcMEPs. Massive hemorrhage reduced the amplitudes of both TeMEPs and TcMEPs in the bilateral lower limbs and this reduction was not reversed by fluid resuscitation. Following bolus administration of remimazolam or propofol, TcMEPs were markedly suppressed, whereas TeMEPs remained unchanged.
CONCLUSIONS: Similar to TcMEPs, TeMEPs amplitudes may decrease after hemorrhage, and this suppression is not reversed by fluid resuscitation. However, unlike TcMEPs, TeMEPs are resistant to transient anesthetic deepening, suggesting that the observed suppression may be attributable to reduced oxygen delivery to the spinal cord rather than to anesthetic deepening.
METHODS: Twelve swine (26.0 ± 0.5 kg) were anesthetized with 8-13% desflurane during preparation and then switched to propofol and remifentanil anesthesia. After baseline measurements, 700 mL of blood was withdrawn over 30 min to induce hypovolemia. Hypovolemia was then treated with 700 mL of hydroxyethyl starch for 30 min (fluid resuscitation). Subsequently, 5 mg of remimazolam was administered, followed by 50 mg of propofol after the effects of remimazolam had reversed. TcMEPs and TeMEPs were recorded at the end of each condition and immediately before and after the administration of remimazolam or propofol.
RESULTS: In all conditions and in all limbs, TeMEPs' amplitudes were greater than those of TcMEPs. Massive hemorrhage reduced the amplitudes of both TeMEPs and TcMEPs in the bilateral lower limbs and this reduction was not reversed by fluid resuscitation. Following bolus administration of remimazolam or propofol, TcMEPs were markedly suppressed, whereas TeMEPs remained unchanged.
CONCLUSIONS: Similar to TcMEPs, TeMEPs amplitudes may decrease after hemorrhage, and this suppression is not reversed by fluid resuscitation. However, unlike TcMEPs, TeMEPs are resistant to transient anesthetic deepening, suggesting that the observed suppression may be attributable to reduced oxygen delivery to the spinal cord rather than to anesthetic deepening.