Background Sevoflurane postconditioning (SevP) is an effective way in relieving myocardial ischemia/reperfusion (IR) injury, which doesn’t work well in diabetic myocardium unfortunately. Prior studies have noted the importance of increasing oxidative stress in diabetic tissues. Noteworthily, mitochondrial fission mediated by dynamin-related protein 1 (Drp1) is an upstream pathway of reactive oxygen production. Whether Drp1 dependent mitochondrial fission is associated with the ineffectiveness of SevP in diabetic myocardium remains unknown. The aim of this study was to explore the important role of Drp1 in diabetic myocardium and investigate whether Drp1 inhibition could restore the cardioprotective effect of SevP. Methods In the first part, adult male Sprague-Dawley(SD) rats were divided into 6 groups. Rats in diabetic groups were fed with high-fat and high-sugar for 8 weeks, and then received a injection of streptozotocin (35 mg/kg) intraperitoneally. Myocardial IR was induced by 30 min occlusion of left anterior descending branch of coronary artery followed by 120 min reperfusion༎SevP was applied by continuous inhalation of 2.5% sevoflurane 1 min before reperfusion, which lasted for 10 min. In the second part, mdivi-1 was used to investigate whether Drp1 inhibition could restore the cardioprotective effects of SevP in diabetic myocardium against I/R injury. The myocardial infarct size, pathology, mitochondrial ultrastructure, cardiomyocyte apoptosis, total SOD activity, MDA content, and Drp1 expression were detected. Results The diabetic myocardium displayed severer injury with greater infarct size and apoptosis. Up-regulated Drp1 expression concomitant with increased mitochondrial fission and oxidative stress were observed in diabetic myocardium subjected to I/R. The deteriorated changes were alleviated in normal but not in diabetic rats. Importantly, mdivi-1 administration significantly suppressed mitochondrial fission and oxidative stress, and the beneficial effects of SevP were restored by mdivi-1. Conclusions The present study indicates a crucial role of Drp1 dependent mitochondrial fission in diabetic myocardium subjected to IR. Drp1 inhibition may be effective in restoring the effect of SevP in reducing diabetic myocardial IR injury.
Objective: This study aimed to investigate the efficacy and safety of extrapleural block (EPB) application in patients with coronary artery disease after thoracoscopic surgery. Methods:Patients with typical symptoms of angina and myocardial ischemia who underwent thoracoscopic surgery at our institution between December 2018 and December 2020 were screened for eligibility and they received paravertebral blocking (PVB), EPB, and patient-controlled intravenous analgesia (PCIA). Visual analog scale (VAS) scores were used to assess the analgesic effect and safety outcomes included heart rate, incidence of postoperative rescue analgesics, cardiac complications, and adverse reactions such as nausea and vomiting.Results: In total, 76 patients (age: 66.5 [61.3, 71] years; male: 63.2%) were eligible, including the PVB group (n = 22), EPB group (n = 25), and PVIA group (n = 29) with comparable baseline characteristics. There was a significantly higher proportion of patients with a VAS score of 1 in the EPB group compared with the other groups at 4 h (88.0% vs. 10.3% for PCIA and 45.5% for PVB; p < .001) and 6 h after the surgery (32.0% vs. 3.4% for PCIA and 13.6% for PVB; p = .012). The preoperative heart rate in the EPB group (81 [71, 94] beats/min) was slightly higher than those in the PVB (76 [70, 85] beats/min) and PCIA groups (76 [69, 84 beats/min]) but without significant difference (p = .193). There was no significant difference in the incidence of rescue analgesia, adverse events, and cardiac complications among the three groups (p = .296, .808, and .669, respectively.) Conclusion:Compared with PVB and PCIA, the EPB could more effectively relieve acute pain after thoracoscopic surgery in patients with coronary artery disease and offer comparable safety benefits in the management of postoperative heart rate, adverse events, and cardiac complications.
The pathogenesis of mitochondrial myopathy, encephalopathy, lactic acidosis and stroke like episodes (MELAS) syndrome has not been fully elucidated. The m.3243A > G mutation which is responsible for 80% MELAS patients affects proteins with undetermined functions. Therefore, we performed quantitative proteomic analysis on skeletal muscle specimens from MELAS patients. We recruited 10 patients with definitive MELAS and 10 age- and gender- matched controls. Proteomic analysis based on nanospray liquid chromatography-mass spectrometry (LC-MS) was performed using data-independent acquisition (DIA) method and differentially expressed proteins were revealed by bioinformatics analysis. We identified 128 differential proteins between MELAS and controls, including 68 down-regulated proteins and 60 up-regulated proteins. The differential proteins involved in oxidative stress were identified, including heat shock protein beta-1 (HSPB1), alpha-crystallin B chain (CRYAB), heme oxygenase 1 (HMOX1), glucose-6-phosphate dehydrogenase (G6PD) and selenoprotein P. Gene ontology and kyoto encyclopedia of genes and genomes pathway analysis showed significant enrichment in phagosome, ribosome and peroxisome proliferator-activated receptors (PPAR) signaling pathway. The imbalance between oxidative stress and antioxidant defense, the activation of autophagosomes, and the abnormal metabolism of mitochondrial ribosome proteins (MRPs) might play an important role in m.3243A > G MELAS. The combination of proteomic and bioinformatics analysis could contribute potential molecular networks to the pathogenesis of MELAS in a comprehensive manner.
Glucagon-like peptide-1 (GLP-1) is a multifunctional hormone with broad pharmacological potential to control inflammation, protect cardiovascular, kidney, and liver functions. Moreover, GLP-1 can also cross the blood-brain barrier and bind with GLP-1R distributed in various parts of the brain, thereby reducing apoptosis caused by neuroinflammation and oxygen stress, and promoting learning, memory, cognitive function, neuroprotection, and nerve cell remodeling. However, the exact molecular pathway by which GLP-1 receptor agonists (GLP-1RAs) exerts protective effects on many organs is not fully understood, so it is a hot topic of research. In this article, the recent research on the multi-organ protection of GLP-1 is reviewed, with emphasis on the research progress in the field of nervous system and perioperative anesthesia.
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