Journal of Oral Tissue Engineering

ORIGINAL ARTICLE
 Sevoflurane Increases p38 Mitogen Activated Protein Kinase Phosphorylation During Ischemia, but its Cardioprotective Effect is not Blocked by SB 203580

 Masami MIYAMAE1, Kazuhiro KANEDA2, Yoshitaka INAMURA2, Mayumi SHIOMI3, Shizuka KOSHINUMA2, Yoshihiro MOMOTA2 and Vincent M. FIGUEREDO4
1Department of Internal Medicine, Osaka Dental University, Osaka, Japan
2Department of Anesthesiology, Osaka Dental University, Osaka, Japan
3Department of Anesthesiology, Osaka Medical College, Takatsuki, Japan
4Institute for Heart and Vascular Health, Einstein Medical Center,
and Jefferson Medical College, Philadelphia, USA
J Oral Tissue Engin 2013;11(1):17-28
SYNOPSIS
It remains unclear whether p38 mitogen activated protein kinase (p38 MAPK) is involved in anesthetic preconditioning (APC). We investigated the effect of inhibiting p38 MAPK activation on sevoflurane-induced APC. Isolated perfused guinea pig hearts underwent 30 min ischemia and 120 min reperfusion. APC was elicited with 2% sevoflurane administration. Inhibition of p38 MAPK was achieved using SB203580. Contractile recovery was monitored by left ventricular developed (LVDP) and end-diastolic (LVEDP) pressure. Infarct size was determined by triphenyltetrazolium chloride stain. Expression of p38 MAPK was determined by Western blot. After ischemia/reperfusion, APC hearts had higher LVDP and lower LVEDP compared to CTL. Infarct size was significantly reduced in APC. SB203580 administration failed to abolish APC. Western blot analysis demonstrated that phosphorylation of p38 MAPK was increased by APC, which was enhanced by SB 203580.
In conclusion, sevoflurane increases p38 MAPK phosphorylation but this is not required for APC.

Key words: sevoflurane, preconditioning, p38 MAPK, SB203580