Pressure reversal of anaesthesia: a synaptic mechanism.
Pressure reversal of anaesthesia: a synaptic mechanism.
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麻醉压力逆转：突触机制。
DOI：
10.1093/bja/60.7.806
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发表时间：
1988
影响因子：
9.8
通讯作者：
MacIver,MB
中科院分区：
文献类型：
--
作者：
Kendig,JJ;Grossman,Y;MacIver,MB
高压诱发癫痫发作并增加麻醉需求（“麻醉压力逆转”），但压力和麻醉剂都抑制兴奋性突触传递。本研究试图解决这一矛盾。氦压力至10.1 MPa与麻醉剂（戊巴比酮）的相互作用。研究了甲壳类动物谷氨酰胺能兴奋性神经肌肉接点对甲氧基氟醚（halothane, methoxyflurane）的抑制作用。压力和麻醉均抑制单次兴奋性连接电位（EJP）。在重复刺激过程中，压力和戊巴比酮都通过增强强直增强来对抗它们自身的抑制作用。10.1 MPa的添加剂增强足以使戊巴比酮抑制反应高于相应的常压水平。在EJP的振幅和时间进程、促进、增强或抑制等方面，压力与任何麻醉药均无明显的拮抗作用。可加性而非拮抗性是该模型突触麻醉抑郁压力逆转的基础。因此，功能性拮抗作用是间接的，可能涉及压力和麻醉的多个作用部位。
Hyperbaric pressure induces seizures and increases anaesthetic requirements (“pressure reversal of anaesthesia ”), but both pressure and anaesthetic agents depress excitatory synaptic transmission. The present study has attempted to resolve this paradox. The interaction between helium pressure to 10.1 MPa and anaesthetic agents (pentobarbitone. halothane, methoxyflurane) was investigated at a crustacean glutaminergic excitatory neuromuscular junction which can be modulated by GABA inhibition. Both pressure and the anaesthetics depressed the singly evoked excitatory junctional potential (EJP). During repetitive stimulation, both pressure and pentobarbitone antagonized their own depressant effects by enhancing tetanic potentiation. The additive enhancement at 10.1 MPa was sufficient to increase the pentobarbitone-depressed response above the corresponding normobaric level. No significant antagonism between pressure and any of the anaesthetics was observed on the properties of EJP amplitude and time course, facilitation, potentiation or inhibition. Additivity rather than antagonism is the basis for pressure reversal of anaesthetic depression at this model synapse. The functional antagonism is therefore indirect, and probably involves multiple sites of action for both pressure and anaesthetics.