PubMed · 626433
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
H Yanagida. 1978. EEG changes during anesthesia.. https://doi.org/10.1097/00000542-197803000-00015
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Explore the source record for details and available documents.
The effects of the volatile anesthetic enflurane on voltage-gated ionic currents of bovine adrenal chromaffin cells were studied using the patch clamp technique. Bath application of 3.5% (1.7 mM) enflurane decreased the outward Ca(2+)-dependent K+ current (IK(Ca)) 'hump' by 88 +/- 6% (mean +/- S.E.M., n = 5 cells) and the peak inward Ca2+ current by 60 +/- 3% (n = 5), whereas the Ca(2+)-independent K+ current fell by only 34 +/- 3% (n = 5) and peak inward Na+ current was unchanged. Exposure of excised patch 'BK' Ca(2+)-dependent K+ channels to 3.5% enflurane revealed that the anesthetic directly suppressed the channel probability of opening by 68 +/- 10% (n = 4) with no effect on open state conductance. The differential sensitivity of depolarizing and hyperpolarizing current pathways may contribute to the biphasic response, excitation and depression, observed in certain neuronal systems in response to this inhalational anesthetic.
We investigated the beta 2-adrenoceptor-mediated effects of atrial and ventricular effective refractory period (ERP), SA node pacemaker activity, and AV conductivity induced by sympathetic nerve stimulation or epinephrine infusion in anesthetized dogs. A beta 2-adrenoceptor antagonist, ICI 118,551 up to 100 micrograms/kg, i.v., inhibited the positive chronotropic and dromotropic responses to sympathetic stimulation but did not shorten the atrial or ventricular ERP, ICI 118,551 also attenuated the positive chronotropic and dromotropic responses and the shortening of atrial ERP in response to epinephrine but not the shortening of ventricular ERP. A selective beta 1-adrenoceptor antagonist, atenolol, inhibited each electrical cardiac response to sympathetic stimulation and epinephrine infusion in a similar manner. These results suggest that beta 2-adrenoceptor-mediated electrical cardiac responses to endogenous catecholamines also exist in addition to the predominant beta 1-adrenoceptor-mediated responses, and that the order of the proportion of beta 2-adrenoceptor-mediated cardiac effects was SA node pacemaker activity much greater than AV conductivity = atrial ERP much greater than ventricular ERP in the dog heart.