Volume 29, Issue 2 e12934
ORIGINAL ARTICLE

Propofol inhibits carbachol-induced chloride secretion by directly targeting the basolateral K+ channel in rat ileum epithelium

S.-H. Tang

S.-H. Tang

Department of Anesthesiology, Qilu Hospital, Shandong University, Jinan, China

These authors contributed equally to this work.Search for more papers by this author
H.-Y. Wang

H.-Y. Wang

Department of Physiology, School of Medicine, Shandong University, Jinan, China

These authors contributed equally to this work.Search for more papers by this author
H. Sun

H. Sun

Department of Thoracic Surgery, Shandong Tumor Hospital, Shandong University, Jinan, China

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N. An

N. An

Department of Physiology, School of Medicine, Shandong University, Jinan, China

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L. Xiao

L. Xiao

Department of Physiology, School of Medicine, Shandong University, Jinan, China

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Q. Sun

Q. Sun

Department of Physiology, School of Medicine, Shandong University, Jinan, China

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D.-B. Zhao

Corresponding Author

D.-B. Zhao

Department of Thoracic Surgery, Shandong Tumor Hospital, Shandong University, Jinan, China

Correspondence

Dong-Bo Zhao, MD, PhD, Department of Thoracic Surgery, Shandong Tumor Hospital, Jinan, China.

Email: [email protected]

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First published: 30 August 2016

Abstract

Background

Propofol is a widely used intravenous general anesthetic. Acetylcholine (ACh) is critical in controlling epithelial ion transport. This study was to investigate the effects of propofol on ACh-evoked secretion in rat ileum epithelium.

Methods

The Ussing chamber technique was used to investigate the effects of propofol on carbachol (CCh)-evoked short-circuit currents (Isc).

Key Results

Propofol (10−2–10−6 mol/L) attenuated CCh-evoked Isc of rat ileum mucosa in a dose-dependent manner. The inhibitory effect of propofol was only evident after application to the serosal side. Pretreatment with tetrodotoxin (TTX, 0.3 μmol/L, n=5) had no effect on propofol-induced inhibitory effect, whereas serosal application of K+ channel inhibitor, glibenclamide, but not, an ATP-sensitive K+ channel inhibitor, largely reduced the inhibitory effect of propofol. In addition, pretreatment with either hexamethonium bromide (HB, nicotinic nACh receptor antagonist) or Cl channel blockers niflumic acid and cystic fibrosis transmembrane conductance regulator (inh)-172 did not produce any effect on the propofol-induced inhibitory effect.

Conclusions & Inferences

Propofol inhibits CCh-induced intestinal secretion by directly targeting basolateral K+ channels.

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