TY - JOUR
T1 - Blockade of anaesthetic-induced preconditioning in the hyperglycaemic myocardium - The regulation of different mitogen-activated protein kinases
AU - Weber, Nina C.
AU - Goletz, Christine
AU - Huhn, Ragnar
AU - Grueber, Yvonne
AU - Preckel, Benedikt
AU - Schlack, Wolfgang
AU - Ebel, Dirk
PY - 2008
Y1 - 2008
N2 - Preconditioning by volatile anaesthetics is blocked by hyperglycaemia. The regulation of mitogen-activated protein kinases during this effect has yet not been investigated. For infarct size measurements, anaesthetized rats were subjected to 25 min coronary artery occlusion followed by 120 min reperfusion. Control animals were not further treated. One group was preconditioned by two 5-min periods of desflurane inhalation (desflurane preconditioning, Des-preconditioning, 1 MAC), each followed by 10-min washout. Four groups received glucose 50% in order to achieve blood glucose concentrations between 22.2 and 33.3 mM/l. Glucose infusion started 40 min before ischaemia (early hyperglycaemia, EH) and stopped with the onset of artery occlusion with (EH+Des-preconditioning) or without (EH) preconditioning. The other two groups received glucose during ischaemia (late hyperglycaemia, LH), again with (LH+Des-preconditioning) or without ((LH) preconditioning. Additional hearts were excised for Western blot of mitogen-activated protein kinases. Infarct size was reduced from 51.7 +/- 9.0% in controls to 28.8 +/- 11.8% after Des-preconditioning (P <0.01 vs Con). Hyperglycaemia alone did not affect infarct size (EH, 51.5 +/- 9.0%, LH, 44.3 +/- 16.9%), but EH as well as LH blocked Des-preconditioning (49.1 +/- 12.3%, P <0.01, 48.1 +/- 17.6%, P <0.05 vs Des-preconditioning). All three mitogen-activated protein kinases showed a similar time course pattern of phosphorylation in the Despreconditioning, EH and EH+Des-preconditioning group. Despite the lack of cardioprotection, mitogen-activated protein kinases are activated in hyperglycaemic myocardium. Therefore, it can be assumed that the hyperglycaemic induced blockade of Des-preconditioning is situated downstream or in parallel of these mitogen-activated protein kinases or involves different signal transduction pathways. (C) 2008 Elsevier B.V. All rights reserved
AB - Preconditioning by volatile anaesthetics is blocked by hyperglycaemia. The regulation of mitogen-activated protein kinases during this effect has yet not been investigated. For infarct size measurements, anaesthetized rats were subjected to 25 min coronary artery occlusion followed by 120 min reperfusion. Control animals were not further treated. One group was preconditioned by two 5-min periods of desflurane inhalation (desflurane preconditioning, Des-preconditioning, 1 MAC), each followed by 10-min washout. Four groups received glucose 50% in order to achieve blood glucose concentrations between 22.2 and 33.3 mM/l. Glucose infusion started 40 min before ischaemia (early hyperglycaemia, EH) and stopped with the onset of artery occlusion with (EH+Des-preconditioning) or without (EH) preconditioning. The other two groups received glucose during ischaemia (late hyperglycaemia, LH), again with (LH+Des-preconditioning) or without ((LH) preconditioning. Additional hearts were excised for Western blot of mitogen-activated protein kinases. Infarct size was reduced from 51.7 +/- 9.0% in controls to 28.8 +/- 11.8% after Des-preconditioning (P <0.01 vs Con). Hyperglycaemia alone did not affect infarct size (EH, 51.5 +/- 9.0%, LH, 44.3 +/- 16.9%), but EH as well as LH blocked Des-preconditioning (49.1 +/- 12.3%, P <0.01, 48.1 +/- 17.6%, P <0.05 vs Des-preconditioning). All three mitogen-activated protein kinases showed a similar time course pattern of phosphorylation in the Despreconditioning, EH and EH+Des-preconditioning group. Despite the lack of cardioprotection, mitogen-activated protein kinases are activated in hyperglycaemic myocardium. Therefore, it can be assumed that the hyperglycaemic induced blockade of Des-preconditioning is situated downstream or in parallel of these mitogen-activated protein kinases or involves different signal transduction pathways. (C) 2008 Elsevier B.V. All rights reserved
U2 - https://doi.org/10.1016/j.ejphar.2008.07.010
DO - https://doi.org/10.1016/j.ejphar.2008.07.010
M3 - Article
C2 - 18655783
SN - 0014-2999
VL - 592
SP - 48
EP - 54
JO - European journal of pharmacology
JF - European journal of pharmacology
IS - 1-3
ER -