Lotz C.,Bayerische Julius Maximilians University |
Fisslthaler B.,Goethe University Frankfurt |
Redel A.,Bayerische Julius Maximilians University |
Smul T.M.,Bayerische Julius Maximilians University |
And 6 more authors.
Journal of Cardiothoracic and Vascular Anesthesia | Year: 2011
Objectives: Myocardial ischemia is accompanied by a rapid activation of adenosine-monophosphateactivated protein kinase (AMPK). However, it is unclear whether this represents a potentially beneficial or detrimental event in the course of ischemic injury. The role of AMPK activation in the cardioprotective setting of desflurane-induced preconditioning has not been investigated to date. Hence, the current study was undertaken to address the role of AMPK activation during desflurane-induced preconditioning in vivo. Design: A prospective randomized vehicle-controlled study. Setting: A university research laboratory. Subjects: Male New Zealand white rabbits (n = 44). Interventions: The animals were subjected to a 30-minute coronary artery occlusion (CAO) followed by 3 hours of reperfusion. Desflurane (1.0 minimum alveolar concentration) was administered for 30 minutes and discontinued 30 minutes prior to CAO. Different groups of animals received the AMPK activator, 5-aminoimidazole-4-carboxamide-1- b-riboside (AICAR), alone or in combination with desflurane. Infarct size was determined gravimetrically; AMPK activity and myocardial glycogen content were measured using specific assays. Phosphorylation of the AMPK substrate, acetyl-CoA carboxylase, was assessed by immunoblotting. Data are mean ± standard error of the mean. Results: Desflurane significantly reduced the myocardial infarct size (36.7 ± 1.9%, p < 0.05) compared with the control group (61.6% ± 3.0%), concomitant with increased myocardial tissue levels of glycogen (2.09 ± 0.07 μg, p < 0.05). Activation of the AMPK by AICAR alone did not protect against ischemic injury (65% ± 3.3), but did abolish the cardioprotection elicited by desflurane (61.8% ± 4.2%) at the same time as increasing myocardial glycogen consumption (1.42 ± 0.15 μg/mL). Conclusions: The results obtained show that the pharmacologic activation of AMPK abolishes cardioprotection elicited by desflurane. © 2011 Elsevier Inc. Source
Vince G.H.,Bayerische Julius Maximilians University |
Bendszus M.,University of Heidelberg |
Westermaier T.,Bayerische Julius Maximilians University |
Solymosi L.,Bayerische Julius Maximilians University |
And 2 more authors.
British Journal of Neurosurgery | Year: 2010
Trigeminal neuralgia in Chiari's type I malformation is rare and remains a therapeutic challenge. We report a case of bilateral trigeminal neuralgia in Chiari's type I malformation. This case demonstrates that microvascular decompression can be an effective treatment strategy for this complex pathology. © 2010 The Neurosurgical Foundation. Source