Signaling pathways involved in desflurane-induced postconditioning in human atrial myocardium in vitro

21Citations
Citations of this article
27Readers
Mendeley users who have this article in their library.

Abstract

BACKGROUND:: Isoflurane and sevoflurane have been shown to elicit myocardial postconditioning, but the effect of desflurane remain unknown. The authors studied the mechanisms involved in desflurane-induced myocardial postconditioning. METHODS:: Contracting isolated human right atrial trabeculae (34°C, stimulation frequency 1 Hz) were exposed to 30-min hypoxia followed by 60-min reoxygenation. Desflurane at 3%, 6%, and 9% was administered during the first 5-min of reoxygenation. Postconditioning with 6% desflurane was studied in the presence of 1 μm calphostin C, a protein kinase C inhibitor; 800 mm 5-hydroxydecanoate, a mitochondrial adenosine triphosphate-sensitive potassium channels antagonist; 1 μm Akt inhibitor; 20 μm PD89058, an extracellular-regulated kinase 1/2 inhibitor; and 1 μm SB 202190, a p38 mitogen-activated protein kinase inhibitor. The force of contraction at the end of the 60-min reoxygenation period was compared (mean ± SD). The p38 mitogen-activated protein kinase phosphorylation was studied using Western blotting. RESULTS:: Desflurane at 3% (77 ± 10% of baseline), 6% (90 ± 14% of baseline), and 9% (86 ± 11% of baseline) enhanced the recovery of force after 60 min of reoxygenation as compared with the control group (51 ± 9% of baseline; P < 0.001). Calphostin C (55 ± 3% of baseline), 5-hydroxydecanoate (53 ± 3% of baseline), Akt inhibitor (57 ± 8% of baseline), PD89058 (64 ± 6% of baseline), and SB 202190 (61 ± 3% of baseline) abolished desflurane-induced postconditioning. Western blot analysis showed that 6% desflurane increased p38 mitogen-activated protein kinase phosphorylation. CONCLUSIONS:: In vitro, desflurane postconditioned human atrial myocardium through protein kinase C activation, opening of mitochondrial adenosine triphosphate-sensitive potassium channels, Akt and extracellular-regulated kinase 1/2 activation, and p38 mitogen-activated protein kinase phosphorylation. © 2008, the American Society of Anesthesiologists, Inc.

References Powered by Scopus

Inhibition of myocardial injury by ischemic postconditioning during reperfusion: Comparison with ischemic preconditioning

1985Citations
N/AReaders
Get full text

Postconditioning the human heart

944Citations
N/AReaders
Get full text

Cardiac muscle cell hypertrophy and apoptosis induced by distinct members of the p38 mitogen-activated protein kinase family

755Citations
N/AReaders
Get full text

Cited by Powered by Scopus

The mechanisms of cardio-protective effects of desflurane and sevoflurane at the time of reperfusion: Anaesthetic post-conditioning potentially translatable to humans?

51Citations
N/AReaders
Get full text

Morphine Postconditioning Protects against Reperfusion Injury via Inhibiting JNK/p38 MAPK and Mitochondrial Permeability Transition Pores Signaling Pathways

23Citations
N/AReaders
Get full text

Argon Exposure Induces Postconditioning in Myocardial Ischemia-Reperfusion

23Citations
N/AReaders
Get full text

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Cite

CITATION STYLE

APA

Lemoine, S., Beauchef, G., Zhu, L., Renard, E., Lepage, O., Massetti, M., … Hanouz, J. L. (2008). Signaling pathways involved in desflurane-induced postconditioning in human atrial myocardium in vitro. Anesthesiology, 109(6), 1036–1044. https://doi.org/10.1097/ALN.0b013e31818d6b09

Readers' Seniority

Tooltip

PhD / Post grad / Masters / Doc 11

48%

Professor / Associate Prof. 7

30%

Researcher 5

22%

Readers' Discipline

Tooltip

Medicine and Dentistry 15

75%

Agricultural and Biological Sciences 3

15%

Sports and Recreations 1

5%

Arts and Humanities 1

5%

Save time finding and organizing research with Mendeley

Sign up for free