Sodium channel isoform‐specific effects of halothane: protein kinase C co‐expression and slow inactivation gating

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Structured PICO

Population

Xenopus oocytes expressing Na channel alpha-subunits (rat skeletal muscle, rat brain, and human cardiac muscle)

Intervention

Halothane (up to 1.0 mM) with co-expression of a constitutively active PKC alpha-isozyme

Comparator

Na channels expressed alone without halothane or without PKC co-expression

Outcome

Macroscopic Na current decay and charge movement assessed via cell-attached patch clamp recordingssurrogate

Halothane exerts isoform-specific suppression of sodium channels, affecting skeletal and brain but not cardiac isoforms, in a PKC-dependent manner.

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May support halothane's cardiac Na channel sparing in animal models; hypothesis-generating for isoform selectivity, pending human studies.

Patel et al. (2000) studied this question.

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May support halothane's cardiac Na channel sparing in animal models; hypothesis-generating for isoform selectivity, pending human studies.