Freye E, Buhl R, Schenk G K
Department of Central Diagnostics, University Clinics of Psychiatry, Essen, Federal Republic of Germany.
Funct Neurol. 1987 Jul-Sep;2(3):281-92.
Alfentanil, a mu-opioid receptor ligand, induced a dose-related suppression of the early N50 peak and an increase in latency of the late N140 peak. The highest dose blocked all potentials. These effects were reversible by naloxone. The kappa-ligand bremazocine, induced a dose-related increase in latency of the late P150 peak which was, however, reversed by the specific kappa-antagonist Mr2266, not by naloxone. Continuous blockade of the mu-receptor with low-dose naloxone topped with cumulative doses of nalbuphine, a mixed narcotic analgesic, resulted in a Mr 2266-reversible increase in latency of the late N100 peak. Influences of the opioids on the SEP may account for their difference in clinical effects.
阿芬太尼，一种μ-阿片受体配体，可引起早期N50波峰的剂量相关性抑制以及晚期N140波峰潜伏期的延长。最高剂量可阻断所有电位。这些效应可被纳洛酮逆转。κ-配体布瑞马唑辛可引起晚期P150波峰潜伏期的剂量相关性延长，然而，这种延长可被特异性κ-拮抗剂Mr2266逆转，而不能被纳洛酮逆转。用低剂量纳洛酮持续阻断μ-受体，再叠加累积剂量的纳布啡（一种混合麻醉性镇痛药），可导致晚期N100波峰潜伏期出现Mr2266可逆性延长。阿片类药物对体感诱发电位的影响可能解释了它们在临床效果上的差异。
