Desflurane-induced Preconditioning against Myocardial Infarction Is Mediated by Nitric Oxide

Smul, Thorsten M.; Lange, Markus; Redel, Andreas; Burkhard, Natalie; Roewer, Norbert; Kehl, Franz

doi:10.1097/00000542-200610000-00018

Cited by 36 publications

(17 citation statements)

References 28 publications

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“…However, the precise threshold and duration that must be achieved to trigger the protective effect has not been established. For APC in particular there is certain evidence that the reduction of ischemia-reperfusion injuries depends on timing and the threshold of repetitive application [4,8]. Our proteomics data underline the impact of repetitive agent application as demonstrated by the cumulative effect of protein changes (Fig.…”

Section: Discussionmentioning

confidence: 54%

“…Modern volatile anaesthetics as elicitors of cardiac preconditioning have been effectively demonstrated in cell culture experiments [1,2] and animal models [3,4,5,6]. There is also supporting evidence from clinical studies that anaesthetic-induced preconditioning (APC) is protective in the clinical setting [7,8,9].…”

Section: Introductionmentioning

confidence: 99%

“…Subsequent molecular investigations of DES-PC were conducted with focus on specific targets known from IPC [2,3,4,5,11,12] but the overall picture of the underlying mechanisms is still lacking. A couple of studies even showed that the signalling pathways may differ from IPC [6,13].…”

Section: Introductionmentioning

confidence: 99%

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In VivoDesflurane Preconditioning Evokes Dynamic Alterations of Metabolic Proteins in the Heart - Proteomic Insights Strengthen the Link between Bioenergetics and Cardioprotection

Dyballa-Rukes

Schuh

Vogt

et al. 2014

Cell Physiol Biochem

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Background: The cardioprotective effect of anaesthetic preconditioning as measured by reduction of ischaemia-reperfusion (I/R) injury is a well described phenomenon. However little is known about the impact on the myocardial proteome. We therefore investigated proteome dynamics at different experimental time points of a preconditioning protocol. Methods: Using an in vivo rat model of desflurane-induced preconditioning (DES-PC) cardiac tissue proteomes were analysed by a gel-based comparative approach. Treatment-dependent protein alterations were assessed by intra-group comparisons. Proteins were identified by mass-spectrometry. Results: A total of 40 protein spots were altered during the 30-minutes lasting preconditioning protocol. None of the proteins was differentially regulated consistently at all experimental time points. Interestingly, 1) the repeated administration of desflurane mostly accounted for proteome alterations during DES-PC, 2) the majority of altered protein species showed a decrease in abundance, 3) these changes primarily affected metabolic proteins involved in NADH/NAD⁺ redox balance, calcium homeostasis and acidosis and 4) protein alterations were not exclusively due to expression changes but also represented modifications of specific protein isoforms. Conclusion: DES-PC evokes dynamic alterations in the cardiac proteome which substantiate a tight regulation of bioenergetic proteins. Unique protein modifications may play a more important role in the preconditioning response.

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Section: Discussionmentioning

confidence: 54%

Section: Introductionmentioning

confidence: 99%

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In VivoDesflurane Preconditioning Evokes Dynamic Alterations of Metabolic Proteins in the Heart - Proteomic Insights Strengthen the Link between Bioenergetics and Cardioprotection

Dyballa-Rukes

Schuh

Vogt

et al. 2014

Cell Physiol Biochem

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“…Infarct size (IS) and area at risk (AAR) were gravimetrically determined as previously described (Smul et al 2006;Lange et al 2008). Briefly, at the end of each experiment, the coronary artery was reoccluded and the AAR determined by infusion of Patent Blue (Sigma-Aldrich, Steinheim, Germany).…”

Section: Measurement Of Myocardial Infarct Sizementioning

confidence: 99%

“…Anaesthetic-induced preconditioning hereby consists of two distinct 'windows': a first 'window' lasting for 2-4 h after the application of the volatile anaesthetic and a second 'window' affording protection after 24 h (Tonkovic-Capin et al 2002). A complex interplay of multiple signalling pathways is known to govern this response, while the increased production of nitric oxide (NO) represents a pivotal element, and inhibition of nitric oxide synthase (NOS) provokes the loss of protection in both windows (Chiari et al 2005;Smul et al 2006). However, the actions preceding the increased NO availability remain elusive, and a number of regulatory factors have been implicated in tuning the NO biosynthesis, such as post-translational modifications, as well as the activation of specific transcription factors (Nathan & Xie, 1994).…”

mentioning

confidence: 99%

Peroxisome-proliferator-activated receptor γ mediates the second window of anaesthetic-induced preconditioning

Lotz¹,

Lange²,

Redel³

et al. 2011

Experimental Physiology

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The second window of anaesthetic-induced preconditioning (APC) is afforded by the interplay of multiple signalling pathways, whereas a similar protective response is mediated by peroxisomeproliferator-activated receptor γ (PPARγ) agonists. However, a possible role of this nuclear receptor during APC has not been studied to date. We investigated the hypothesis that the second window of APC is mediated by the activation of PPARγ. New Zealand White rabbits (n = 48) were subjected to 30 min of coronary artery occlusion followed by 3 h of reperfusion. The animals received desflurane (1.0 minimal alveolar concentration), the PPARγ antagonist GW9662, as well as the combined application of both, respectively, 24 h prior to coronary artery occlusion. Infarct size was determined gravimetrically; tissue levels of 15-deoxy-12,14 -prostaglandin J 2 (15d-PGJ 2 ) and nitrite/nitrate (NO x ), as well as PPAR DNA binding were measured using specific assays. Data are presented as means ± s.e.m. Desflurane led to a reduced myocardial infarct size (41.7 ± 2.5 versus 61.8 ± 2.8%, P < 0.05), accompanied by significantly increased PPAR DNA binding (289.9 ± 33 versus 102.9 ± 18 relative light units, P < 0.05), as well as elevated tissue levels of 15d-PGJ 2 (224.4 ± 10.2 versus 116.9 ± 14.2 pg ml −1 , P < 0.05) and NO x (14.9 ± 0.7 versus 5.4 ± 0.7 μm, P < 0.05). Pharmacological inhibition of PPARγ abolished these protective effects, resetting the infarct size (56.5 ± 2.9%), as well as PPAR DNA-binding activity (91.2 ± 31 relative light units) and NO x tissue levels (5.9 ± 0.9 μm) back to control levels. Desflurane governs a second window of APC by increasing the production of 15d-PGJ 2 , subsequently activating PPARγ, resulting in a diminished myocardial infarct size by increasing the downstream availability of NO.

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Cardiovascular Effects of Anesthetics, Sedatives, Postoperative Analgesic Agents, and Other Pharmaceuticals

Gross

2009

Animal Models in Cardiovascular Research

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Desflurane-induced Preconditioning against Myocardial Infarction Is Mediated by Nitric Oxide

Cited by 36 publications

References 28 publications

In VivoDesflurane Preconditioning Evokes Dynamic Alterations of Metabolic Proteins in the Heart - Proteomic Insights Strengthen the Link between Bioenergetics and Cardioprotection

In VivoDesflurane Preconditioning Evokes Dynamic Alterations of Metabolic Proteins in the Heart - Proteomic Insights Strengthen the Link between Bioenergetics and Cardioprotection

Peroxisome-proliferator-activated receptor γ mediates the second window of anaesthetic-induced preconditioning

Cardiovascular Effects of Anesthetics, Sedatives, Postoperative Analgesic Agents, and Other Pharmaceuticals

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