PMID: 9447865Feb 3, 1998Paper

Sensitization of the cardiac Na channel to alpha1-adrenergic stimulation by inhalation anesthetics: evidence for distinct modulatory pathways

Anesthesiology
H U WeigtZ J Bosnjak

Abstract

Alpha1-adrenergic receptor stimulation has been shown to inhibit cardiac Na+ current (INa). Furthermore, some form of synergistic interaction of alpha1-adrenergic effects on INa in combination with volatile anesthetics has been reported. In this study, the authors investigated the possible role of G proteins and protein kinase C in the effects of halothane and isoflurane in the absence and presence of alpha1-adrenergic stimulation on the cardiac INa. The standard whole-cell configuration of the patch-clamp technique was used. INa was elicited by depolarizing test pulses from a holding potential of -80 mV in reduced Na+ solution (10 mM). The experiments were conducted on ventricular myocytes enzymatically isolated from adult guinea pig hearts. The inhibitory effect of halothane (1.2 mM) and isoflurane (1 mM) on peak INa was significantly diminished in the presence of guanosine 5'-O-[2-thiodiphosphate (GDPbetaS). In myocytes pretreated with pertussis toxin (PTX), the potency of halothane was significantly enhanced, but the isoflurane effect was unchanged. In the presence of the protein kinase C (PKC) inhibitor bisindolylmaleimide (BIS), the effect of halothane was unchanged. In contrast, the effect of isoflurane on INa in the pre...Continue Reading

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Feb 1, 1997·Anesthesia and Analgesia·H U WeigtZ J Bosnjak

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Citations

Apr 23, 2004·Acta Anaesthesiologica Scandinavica·R HünekeA Lückhoff
Mar 17, 1999·Anesthesiology·M S IsmaeilB A Cason
Oct 27, 2005·Anesthesiology·Markus W HollmannMarcel E Durieux
Jun 29, 2002·Anesthesia and Analgesia·Akira KudohTomoko Takazawa
Aug 14, 2002·British Journal of Anaesthesia·M J Rebecchi, S N Pentyala

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