Erector Spinae Plane Block. A narrative review / Bloqueo del plano del músculo erector de la espina. Revisión narrativa de la literatura

Abstract The erector spinae plane (ESP) block is an interfascial block described in 2016 by Forero and collaborators, with wide clinical uses and benefits when it comes to analgesic control in different surgeries. This block consists of the application of local anesthetic (LA) in a deep plane over the transverse process, anterior to the erector spinae muscle in the anatomical site where dorsal and ventral branches of the spinal nerve roots are located. This review will cover its clinical uses according to different surgical models, the existing evidence and complications described to date.

Resumen El bloqueo del plano del músculo erector de la espina (ESP, por sus siglas en inglés) es un bloqueo interfascial descrito en 2016 por Forero y colaboradores, con amplios usos clínicos y beneficios en relación con el control analgésico de diferentes modelos quirúrgicos. Este consiste en la aplicación de anestésico local (AL) en un plano profundo sobre apófisis transversa anterior al músculo erector de la espina, sitio anatómico donde se encuentra la bifurcación de los ramos dorsal y ventral de las raíces nerviosas espinales. En esta revisión, se expondrán los usos clínicos según diferentes modelos quirúrgicos, la evidencia que existe de ellos y las complicaciones descritas hasta la actualidad.

Presentación de caso / Spinal cord reperfusion injury secondary to intradural cervical hernia surgery. A case report

RESUMEN La hernia discal intradural es una condición rara. Los déficits neurológicos posquirúrgicos son complicaciones muy poco frecuentes. La aparición de hiperintensidad medular en la imagen de resonancia magnética posoperatoria, en un paciente con una cirugía sin complicaciones sugiere el diagnóstico de White Cord Syndrome o lesión por reperfusión de la médula espinal. En este artículo se describen las características de una paciente que desarrolló defecto neurológico severo posoperatorio. Con cirugía cervical previa, presentó hernia discal extruida C6-C7 que comprimía el cordón medular. Se realizó disectomía, y se presentó entonces déficit neurológico posoperatorio; otros hallazgos clínicos e imagenológicos llevaron a la reintervención quirúrgica. Al cabo de dos meses presentaba Nurick 5. El White Cord Syndrome resulta una complicación poco frecuente; tanto así que este caso es el primero reportado en Cuba. Su presentación luego de cirugía para un disco intradural no ha sido referida. Se diagnostica por la exclusión de complicaciones transoperatorias, y por hiperintensidad del cordón medular en T2. La fisiopatología está mediada por radicales libres. El manejo se centra en una adecuada descompresión, uso de esteroides y rehabilitación. La identificación precoz de este síndrome es crucial para evitar complicaciones fatales.

ABSTRACT Intradural disc herniation is a rare condition. Post-surgical neurological deficits are very rare complications. The appearance of spinal cord hyperintensity on postoperative magnetic resonance imaging in a patient with uncomplicated surgery suggests a diagnosis of White Cord Syndrome or spinal cord reperfusion injury. This article describes the characteristics of a patient who developed a severe postoperative neurological defect. With previous cervical surgery, presented extruded C6-C7 disc herniation that compressed the spinal cord. Discectomy was performed, and postoperative neurological deficit was then presented; Other clinical and imaging findings led to surgical reintervention. Two months later, she presented Nurick 5. White Cord Syndrome is a rare complication; so much so that this case is the first reported in Cuba. The presentation after surgery for an intradural disc has not been reported. It is diagnosed by the exclusion of intraoperative complications, and by hyperintensity of the spinal cord in T2. The pathophysiology is mediated by free radicals. Management focuses on adequate decompression, steroid use, and rehabilitation. Early identification of this syndrome is crucial to avoid fatal complications.

The Protective Effect of Kaempferol Against Ischemia/Reperfusion Injury Through Activating SIRT3 to Inhibit Oxidative Stress

Abstract Introduction: The objective of this study is to investigate the protective effect of kaempferol against ischemia/reperfusion (IR) injury and the underlying molecular mechanisms. Methods: H9C2 cells were pretreated with kaempferol for 24 hours and further insulted with IR injury. Cell vitality, reactive oxygen species (ROS) level, glutathione (GSH) level, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity, and sirtuin-3 (SIRT3), B-cell lymphoma 2 (Bcl2), and Bcl2-associated X protein (Bax) expressions were evaluated. Moreover, short interfering ribonucleic acid targeting SIRT3 was used to investigate the role of SIRT3 against IR mediated by kaempferol in vitro. IR mice models were also established to confirm the protective effects of kaempferol on IR in vivo. Results: After IR injury, H9C2 cells vitality was reduced, ROS levels, NADPH oxidase activity, and Bax expressions were increased, and GSH levels and Bcl2 expressions were decreased. After kaempferol pretreatment, the vitality of H9C2 cells was increased. The levels of ROS, NADPH oxidase activity, and Bax expression were decreased. In addition, levels of GSH and Bcl2 expression were enhanced. Furthermore, silencing SIRT3 attenuated the protective effect mediated by kaempferol, with increased ROS levels, NADPH oxidase activity, and Bax expression, along with reduced GSH level and Bcl2 expression. In vivo IR model showed that kaempferol could preserve IR-damaged cardiac function. Conclusion: Kaempferol has the capability of attenuating H9C2 cells IR injury through activating SIRT3 to inhibit oxidative stress.

Role of fibrinogen in the attenuation of ischemia reperfusion and remote ischemic preconditioning / El papel del fibrinógeno en la atenuación de la isquemia-reperfusión y el preacondicionamiento isquémico remoto

Abstract Background: Ischemic reperfusion injury (IRI) is a common hazard involved in many human diseases, such as cerebral stroke, myocardial infarction, solid organ transplant dysfunction or failure, and vascular diseases. Understanding the molecular bases of this injury is essential for the prevention and control of these life-threatening conditions. Ischemic and remote ischemic preconditioning techniques (IPC and RIPC, respectively) have gained increasing importance in the clinical practice to protect against the IRI; however, the exact mechanisms of these techniques are not fully understood, which renders their clinical application query. Possible effectors: Nitric oxide (NO) has been reported by multiple studies to be an important mediator of the protective effects of those techniques. While the physiological concentrations of NO and fibrinogen (FB) are known to antagonize each other, the circulating levels of both effectors increase in response to RIPC. Hypothesis: While NO has potential anti-inflammatory effects, non-soluble fibrinogen (sFB) shows pro- inflammatory effects. However, the sFB may have the potential to act synergistically rather than antagonistically with NO toward the attenuation of the IRI. Conclusion: While increased FB is considered a risk factor for cardiovascular and inflammatory conditions that is also able to decrease the efflux of NO, and increase the NO oxidative metabolits and S- nitroglutathione, the increased sFB during the acute phase reaction might have other protective aspects that should be carefully investigated.

Resumen Antecedentes: La lesión por isquemia-reperfusión (LIR) es un riesgo común involucrado en muchas enfermedades humanas tales como derrame cerebral, infarto del miocardio, disfunción o falla de trasplante de órgano sólido, y enfermedades vasculares. Una comprensión de la base molecular de esta lesión es fundamental para la prevención y el control de estas enfermedades potencialmente mortales. Las técnicas de preacondicionamiento isquémico y preacondicionamiento isquémico remoto (PIR) han cobrado una creciente importancia en la práctica clínica para la protección contra la LIR, sin embargo, los mecanismos precisos de estas técnicas no se entienden plenamente, lo cual pone en duda su aplicación clínica. Posibles efectores: El óxido nítrico (ON) ha sido reportado por varios estudios como un importante mediador de los efectos protectores de estas técnicas. Si bien se sabe que las concentraciones fisiológicas del ON y fibrinógeno son antagónicas, los niveles circulantes de ambos efectores aumentan en respuesta al PIR. Hipótesis: Aunque el ON tiene posibles efectos anti-inflamatorios, el fibrinógeno insoluble muestra efectos proinflamatorios. Sin embargo, el fibrinógeno soluble puede tener el potencial de actuar de manera sinérgica en lugar de antagónica con el ON hacia la atenuación de la LIR. Conclusión: Aunque el fibrinógeno elevado se considera un factor de riesgo para las enfermedades cardiovasculares e inflamatorias, que también puede disminuir la descarga de ON y aumentar los niveles de metabolitos oxidantes del ON y de S-nitrosoglutatión, el aumento de fibrinógeno soluble durante la reacción de fase aguda puede tener otros aspectos protectores que deben ser cuidadosamente investigados.

Post-cardiac arrest syndrome in adult hospitalized patients / Síndrome posparo cardiaco en pacientes adultos hospitalizados

Abstract Adult In-hospital Cardiac Arrest (IHCA) is defined as the loss of circulation of an in-patient. Following high-quality cardiopulmonary resuscitation (CPR), if the return of spontaneous circulation (ROSC) is achieved, the post-cardiac arrest syndrome develops (PCAS). This review is intended to discuss the current diagnosis and treatment of PCAS. To approach this topic, a bibliography search was conducted through direct digital access to the scientific literature published in English and Spanish between 2014 and 2020, in MedLine, SciELO, Embase and Cochrane. This search resulted in 248 articles from which original articles, systematic reviews, meta-analyses and clinical practice guidelines were selected for a total of 56 documents. The etiologies may be divided into 56% of in-hospital cardiac, and 44% of non-cardiac arrests. The incidence of this physiological collapse is up to 1.6 cases/1,000 patients admitted, and its frequency is higher in the intensive care units (ICU), with an overall survival rate of 13% at one year. The primary components of PCAS are brain injury, myocardial dysfunction and the persistence of the precipitating pathology. The mainstays for managing PCAS are the prevention of cardiac arrest, ventilation support, control of peri-cardiac arrest arrythmias, and interventions to optimize neurologic recovery. A knowledgeable healthcare staff in PCAS results in improved patient survival and future quality of life. Finally, there is clear need to do further research in the Latin American Population.

Resumen El paro cardiaco intrahospitalario en el adulto (IHCA) se define como el cese de circulación ocurrido dentro de las instalaciones hospitalarias. Después de la reanimación cardiopulmonar (RCP) de alta calidad, si se logra el retorno de circulación espontánea (ROSC), aparece entonces el síndrome posparo cardiaco (SPPC). En esta revisión se pretende presentar el estado actual del diagnóstico y tratamiento del SPPC. Para abordar este tema, se realizó una búsqueda bibliográfica mediante la consulta digital directa de la literatura científica publicada entre 2014 y 2020 en inglés y español recogida en las bases de datos MedLine, SciELO, Embase y Cochrane. La búsqueda inicial arrojó 248 artículos, de los cuales se eligieron artículos originales, revisiones sistemáticas, metaanálisis y guías de práctica clínica, para una selección final de 56 documentos. Las etiologías del paro cardiaco intrahospitalario se pueden dividir en cardiacas y no cardiacas, en el 56 % y 44 %, respectivamente. El colapso fisiológico tiene incidencias de hasta 1,6 casos/1.000 pacientes admitidos, y es más frecuente en las unidades de cuidado intensivo (UCI), con una tasa de supervivencia general de 1 año del 13 %. Los componentes principales del SPPC son la lesión cerebral, la disfunción miocárdica y la persistencia de la patología precipitante. Los pilares del manejo del SPPC son la prevención del paro cardiaco, soporte ventilatorio, control de arritmias periparo cardiaco y las intervenciones para optimizar la recuperación neurológica. El conocimiento del SPPC por parte del personal de la salud ofrece mejor sobrevida y futura calidad de vida a los pacientes. Finalmente, se resalta la clara necesidad de ahondar en mayores investigaciones en la población latinoamericana.

What is the role of heat shock protein in abdominal organ transplantation?

ABSTRACT Ischemia-reperfusion injury is a pathophysiological event occuring after abdominal organ transplantation, and has a significant influence on prognosis and survival of the graft. It is involved in delaying the primary function or non-functioning of the graft. The objective of this study was to provide information on heat shock protein mechanisms in ischemia-reperfusion injuries in abdominal organ transplantations, and to indicate the possible factors involved that may influence the graft outcome. Several classes of heat shock proteins are part of the ischemia and reperfusion process, both as inflammatory agonists and in protecting the process. Studies involving heat shock proteins enhance knowledge on ischemia-reperfusion injury mitigation processes and the mechanisms involved in the survival of abdominal grafts, and open space to support therapeutic future clinical studies, minimizing ischemia and reperfusion injuries in abdominal organ transplantations. Expression of heat shock proteins is associated with inflammatory manifestations and ischemia-reperfusion injuries in abdominal organ transplantations and may influence graft outcomes.

The effects of methanol extract of Galium verum L on cardiac redox state in hypertensive rats

Abstract The aim of this study was to assess the effects of methanol extract of G. verum on redox status of isolated heart of spontaneously hypertensive rats after ischemia. Twenty-four Wistar albino rats were divided into three groups: untreated control rats and rats that received 125 and 250 mg/kg G. verum extract for 4 weeks per os. Index of lipid peroxidation (measured as TBARS) and parameters of antioxidative defence system such as level of reduced glutathione (GSH) and activities of catalase (CAT) and superoxide dismutase (SOD) were spectrophotometrically determined in heart homogenate. The index of lipid peroxidation in heart tissue was lower in both treated groups compared to the control group. On the other hand, the activity of SOD was significantly higher after consumption of both doses, while the activity of CAT was significantly higher only after treatment with a higher dose of extract. Based on our results we might conclude that 4-week treatment with methanol extracts of G. verum has the potential to modulate myocardial redox signaling after ischemia, thus significantly alleviating cardiac oxidative stress and exerting dose-dependent antioxidant properties. Future studies are certainly necessary to fully clarify the role of this plant species in myocardial I-R injury.

Effects of systemic inflammation due to hepatic ischemia-reperfusion injury upon lean or obese visceral adipose tissue

Purpose: To evaluate how the induction of liver damage by ischemia and reperfusion affects the adipose tissue of lean and obese mice. Methods: Lean and diet-induced obese mice were subjected to liver ischemia (30 min) followed by 6 h of reperfusion. The vascular stromal fraction of visceral adipose tissue was analyzed by cytometry, and gene expression was evaluated by an Array assay and by RT-qPCR. Intestinal permeability was assessed by oral administration of fluorescein isothiocyanate (FITC)-dextran and endotoxemia by serum endotoxin measurements using a limulus amebocyte lysate assay. Results: It was found that, after liver ischemia and reperfusion, there is an infiltration of neutrophils, monocytes, and lymphocytes, as well as an increase in the gene expression that encode cytokines, chemokines and their receptors in the visceral adipose tissue of lean mice. This inflammatory response was associated with the presence of endotoxemia in lean mice. However, these changes were not observed in the visceral adipose tissue of obese mice. Conclusions: Liver ischemia and reperfusion induce an acute inflammatory response in adipose tissue of lean mice characterized by an intense chemokine induction and leukocyte infiltration; however, inflammatory alterations are already present at baseline in the obese adipose tissue and liver ischemia and reperfusion do not injure further.

Naringin attenuates acute myocardial ischemia-reperfusion injury via miR126/GSK-3ß/ß-catenin signaling pathway

Introduction: Myocardial ischemia-reperfusion (I/R) injury is one of the mechanisms contributing to the high mortality rate of acute myocardial infarction. Purpose: This study intended to study the role of naringin in cardiac I/R injury. Methods: AC16 cells (human cardiomyocyte cell line) were subjected to oxygen-glucose deprivation/recovery (OGD/R) treatment and/or naringin pretreatment. Then, the apoptosis was examined by flow cytometry and Western blotting. The concentration of IL-6, IL-8 and TNF-α was measured by enzyme-linked immunosorbent assay (ELISA) kits. How naringin influenced microRNA expression was examined by microarrays and quantitative real-time polymerase chain reaction (qRT-PCR). Dual luciferase reporter assay was employed to evaluate the interaction between miR-126 and GSK-3ß. The GSK-3ß/ß-catenin signaling pathway was examined by Western blotting. Finally, rat myocardial I/R model was created to examine the effects of naringin in vivo. Results: Naringin pretreatment significantly decreased the cytokine release and apoptosis of cardiomyocytes exposed to OGD/R. Bioinformatical analysis revealed that naringin upregulated miR-126 expression considerably. Also, it was found that miR-126 can bind GSK-3ß and downregulate its expression, suggesting that naringin could decrease GSK-3ß activity. Next, we discovered that naringin increased ß-catenin activity in cardiomyocytes treated with OGD/R by inhibiting GSK-3ß expression. Our animal experiments showed that naringin pre-treatment or miR-126 agomir alleviated myocardial I/R. Conclusions: Naringin preconditioning can reduce myocardial I/R injury via regulating miR-126/GSK-3ß/ß-catenin signaling pathway, and this chemical can be used to treat acute myocardial infarction.

Tanshinone IIA ameliorates myocardial ischemia/reperfusion injury in rats by regulation of NLRP3 inflammasome activation and Th17 cells differentiation

Purpose: Tanshinone IIA is a well-known lipophilic active constituent refined from traditional Chinese medicines, danshen. It has been previously demonstrated to possess various biological properties, including anti-inflammatory, antioxidant, promoting angiogenesis effect and so on. However, the mechanism of tanshinone IIA on myocardial ischemia-reperfusion injury (MI/RI) remains unclear. In this study, we investigated the effect of tanshinone IIA on MI/RI. Methods: MI/RI rat models were set up. Echocardiographic evaluation and hematoxylin and eosin staining were performed to analyze the cardiac function and morphology of MI/RI. Western blot was conducted for the detection of protein expression of pyrin domain containing 3 (NLRP3) and caspase-1 in heart tissues. Flow cytometry and real-time polymerase chain reaction were used for the detection of proinflammatory cytokines and Th17 cells differentiation. Results: We found that tanshinone IIA alleviated the myocardial damage of MI/RI, ameliorated the overall and local inflammatory reaction, and produced a cardioprotective effect by inhibiting of NLRP3 inflammasome activation and Th17/Treg cells differentiation. Conclusions: Our results highlighted the cardio-protective effect of tanshinone IIA on MI/RI and uncovered its underlying mechanism related to the NLRP3 inflammasome inhibition and the modulation of Th17/Treg cells differentiation.

The protective effects of dietary Clostridium butyricum supplementation on hepatic ischemia reperfusion injury in rats

Purpose: This study investigated the effects of oral administration of Clostridium butyricum (C. butyricum) on inflammation, oxidative stress, and gut flora in rats with hepatic ischemia reperfusion injury (HIRI). Methods: The rats from C. butyricum group were given C. butyricum for 5 days. Then, hepatic ischemia for 30 min and reperfusion for 6 h were performed in all the rats. After the animals were sacrificed, alanine transaminase (ALT), aspartate aminotransferase (AST), lipopolysaccharide (LPS) in serum, short-chain fatty acids (SCFAs), and gut microbiota composition in feces, and malondialdehyde (MDA), glutathione (GSH), tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6), Toll-like receptor 4 (TLR4), nuclear factor-kappa Bp65 (NF-κBp65) and histological analysis in the liver were performed. Results: The rats given C. butyricum showed decreased ALT, AST, LPS, and MDA; improved GSH and histological damage; changes in SCFAs; declined TNF-α, IL-6, TLR4, and pNF-κBp65/NF-κBp65; and changes in the gut microbial composition, which decreased the Firmicutes/Bacteroidetes ratio and increased the relative abundance (RA) of probiotics. Conclusions: C. butyricum supplementation protected against HIRI by regulating gut microbial composition, which contributed to the decreased LPS and attenuation of inflammation and oxidative stress. These indicate C. butyricum may be a potent clinical preoperative dietary supplement for HIRI.

Research progress of nuclear factor E 2-related factor 2 signaling pathway in neuroprotective mechanism of cerebral ischemia/reperfusion injury / 中华危重病急救医学

Cerebral ischemia/reperfusion (I/R) injury refers to an aggravated brain tissue damage caused by the restoration of blood supply after acute ischemia for a period of time. Its pathogenesis is complex, including oxidative stress, inflammatory response, and excitatory amino acid toxicity. The effective clinical treatments of cerebral I/R injury after ischemic stroke (IS) are limited. Nuclear factor E 2-related factor 2 (Nrf2), the most critical antioxidant transcription factor in cells, can coordinate multiple cytoprotective factors to inhibit oxidative stress. Since Nrf2 signaling pathway is considered to be one of the most important cellular defense mechanisms against oxidative stress, targeting Nrf2 intervention has become an attractive therapeutic strategy in the prevention and treatment of cerebral I/R injury. This review focuses on the structure, regulation and function of Nrf2 signaling pathway, as well as its activation and potential therapeutic targets in cerebral I/R injury. The important role and future potential of Nrf2 pathway in the pathogenesis of cerebral I/R injury were discussed.

Effects of trioxygen preconditioning on cerebral ischemia/reperfusion injury and glutamate receptor in rats / 中华危重病急救医学

Objective:To study the effects of trioxygen pretreatment on cerebral ischemia/reperfusion (I/R) injury in rats.Methods:A total of 24 clean grade male Sprague-Dawley (SD) rats were randomly divided into Sham group, brain I/R group (I/R group) and Ozone pretreatment group (Ozone group), with 8 rats in each group. The animals were routinely fed, and the operation was performed 5 days after the intervention of Ozone group by intraperitoneal injection of trioxygen water (concentration 80 mg/L, 0.01 mL/g), and the Sham group and I/R group were injected with equal volume normal saline. The Sham group only separated the arteries without ligation, and the I/R group and Ozone group established the rat cerebral I/R model. Neurological deficit score (NDS) was performed 2 hours after ischemia and modified neurological deficit score (mNSS) was performed 24 hours after reperfusion. Brain tissue was collected after anesthesia. Cerebral infarction was observed by 2, 3, 5-triphenyltetrazolium chloride (TTC) staining and the percentage of cerebral infarction volume was calculated. Protein expression of metabolic glutamate receptor 5 (mGluR5) and ionic glutamate α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor (AMPAR) subunit GluA2 in cerebral ischemic penumbra was determined by Western blotting.Results:Compared with the Sham group, NDS score, mNSS score and percentage of cerebral infarction volume in I/R group were increased [NDS score: 2.63±0.52 vs. 0, mNSS score: 9.63±1.19 vs. 1.13±0.64, cerebral infarction volume: (41.25±2.93)% vs. 0%, all P < 0.05], and expressions of mGluR5 and GluA2 in penumbra area of cerebral ischemia were decreased [mGluR5 protein (mGluR5/β-actin): 0.44±0.14 vs. 1.00±0.10, GluA2 protein (GluA2/β-actin): 0.23±0.08 vs. 1.00±0.25, both P < 0.05]. Compared with the I/R group, mNSS score and percentage of cerebral infarction volume in the Ozone group were decreased [mNSS score: 7.00±1.20 vs. 9.63±1.19, cerebral infarction volume: (27.23±6.21)% vs. (41.25±2.93)%, both P < 0.05], and mGluR5 and GluA2 expressions in the penumbra of cerebral ischemia were up-regulated [mGluR5 protein (mGluR5/β-actin): 0.81±0.10 vs. 0.44±0.14, GluA2 protein (GluA2/β-actin): 0.76±0.13 vs. 0.23±0.08, both P < 0.05]. Conclusion:Trioxygen preconditioning can alleviate cerebral I/R injury in rats, and its mechanism may be related to the upregulation of GluR5 and GluA2 in the ischemic penumbra.

Diagnostic value of electrocardiographic ST-segment changes for myocardial injury related to percutaneous coronary intervention / 中国基层医药

Objective:To investigate the diagnostic value of electrocardiographic ST-segment changes for myocardial injury related to percutaneous coronary intervention.Methods:We included 60 patients who received percutaneous coronary intervention in Haining People's Hospital from January 2020 to February 2021 in this study. We detected serum troponin I level before and after treatment and recorded electrocardiographic ST-segment changes. Taking serum troponin I level as a reference, we divided these patients into myocardial injury and non-myocardial injury groups and analyzed the influential factors of myocardial injury.Results:Balloon inflation time and stent length were (85.6 ± 56.2) minutes and (25.2 ± 15.2) mm in the myocardial injury group, and they were (48.5 ± 39.2) minutes and (17.2 ± 8.2) mm in the non-myocardial injury group. There were no significant differences in balloon inflation time and stent length between the two groups ( t = -3.01, -2.42, both P < 0.05). The proportion of patients with electrocardiographic ST-segment changes was significantly higher in the myocardial injury group than in the non-myocardial injury group [(80.77% (21/26) vs. 5.88% (2/34), χ2= 34.95, P < 0.001). Multivariable logistic regression analysis results showed that electrocardiographic ST-segment changes were an influential factor of myocardial injury ( r = 69.25, P < 0.05). Conclusion:Electrocardiographic ST-segment changes are an independent influential factor of myocardial injury related to percutaneous coronary intervention. It can effectively judge the possibility of developing a myocardial injury and increase the safety of percutaneous coronary intervention.

The role of the fat mass and obesity-associated protein in ischemia-reperfusion injury of human renal tubular epithelial cells / 中华实用儿科临床杂志

Objective:To explore the role of the fat mass and obesity-associated protein (FTO) in human renal tubular epithelial cells (HK-2) suffering ischemia-reperfusion injury (IRI).Methods:The in vitro IRI mo-del was established in HK-2 cells by induction with antimycin A, A23187 and 2-deoxy-D-glucose.The cells were divided into control group and ischemia-reperfusion group (I/R group). The mRNA and protein expressions of FTO, B-cell lymphoma / leukemia 2(Bcl-2)-associated X(Bax), Bcl-2 and cleaved cysteinyl aspartate specific proteinase(cleaved Caspase-3) in HK-2 cells before and after IRI were detected by real-time fluorescent quantitative PCR(qPCR) and Western blot, respectively.Cell apoptosis was measured using flow cytometry.The level ofe N 6-methy-ladenosine (m 6A) RNA was detected by colorimetry. Results:(1) The mRNA expressions of FTO (0.15±0.05 vs.1.00±0.23) and Bcl-2 (0.14±0.07 vs.1.02±0.25) in I/R group were significantly lower than those in control group; While those of Bax (3.10±0.35 vs.1.00±0.13) and cleaved Caspase-3 (4.21±0.56 vs.1.00±0.09) were significantly higher ( t=6.28, 5.84, -9.83, and -9.84, respectively, all P<0.01). (2) The protein expressions of FTO (0.69±0.14 vs.1.37±0.02) and Bcl-2 (0.50±0.12 vs.1.25±0.21) were significantly lower in I/R group than those of control group; While those of Bax (1.04±0.08 vs.0.57±0.06) and cleaved Caspase-3 (0.99±0.05 vs.0.36±0.07) were significantly higher ( t=8.10, 5.49, -8.22, and -12.09, respectively, all P<0.05). (3) Compared with the control group, the apoptosis rate of HK-2 cells in I/R group was significantly higher [(61.70±1.01)% vs.(0.16±0.10)%, t=63.80, P<0.01]. (4) Compared with the control group, the percentage of m 6A modification level in total RNA in I/R group was significantly higher [(3.13±0.21)% vs.(1.10±0.26)%, t=-10.61, P<0.01]. Conclusions:FTO-mediated RNA m 6A modification may affect renal IRI by regulating the apoptosis of HK-2 cells.

Cellular FLICE-like inhibitory protein alleviates myocardial ischemia/reperfusion injury via inhibiting necroptosis / 中华急诊医学杂志

Objective:To explore the regulatory effect of cellular FLICE-like inhibitory protein (cFLIP) on myocardial ischemia-reperfusion injury based on the RIPK1/RIPK3/MLKL-mediated necroptosis pathway.Methods:The cardiomyocyte hypoxia/reoxygenation (H/R) model was constructed by hypoxia for 4 h/reoxygenation for 12 h, and the rat ischemia reperfusion (I/R) model was constructed by ligating the left anterior descending artery for 30 min and reperfusion for 3 h. CCK-8 method was used to detect the viability of cardiomyocytes in each group. DAPI/PI double staining was used to observe changes in necrosis rate of myocardial cell. STRING database was used to predict the protein interaction network of cFLIP. TTC staining was used to detect the area of myocardial infarction in each group of rats, and the protein expression of cFLIPL, cFLIPS, p-RIPK1, p-RIPK3 and p-MLKL were detected by Western blot.Results:In cardiomyocyte H/R injury and myocardial tissue I/R injury, the protein expressions of cFLIPL and cFLIPS were significantly down-regulated, while the levels of p-RIPK1, p-RIPK3 and p-MLKL were increased significantly. Up-regulating the protein expression of cFLIPL and cFLIPS could significantly reduce the damage of cardiomyocytes and the rate of cell necrosis induced by H/R, and decrease the area of myocardial infarction caused by I/R. STRING database results showed that cFLIP had direct protein interactions with RIPK1 and RIPK3. Overexpression of cFLIP in cardiomyocyte and myocardial tissue significantly inhibited H/R or I/R induced the phosphorylation levels of RIPK1, RIPK3 and MLKL.Conclusions:Overexpression of cFLIP can significantly inhibit the RIPK1/RIPK3/MLKL-mediated necroptosis, thereby reducing myocardial cell damage and decreasing the area of myocardial infarction.

Gabapentin alleviates myocardial ischemia-reperfusion injury through the PI3K-AKT signaling pathway / 中华急诊医学杂志

Objective:To evaluate the effect of gabapentin on myocardial ischemia-reperfusion injury and its mechanism.Methods:Sixty male clean SD rats, aged 10 weeks and weighing 250 g~300 g, were divided into 5 groups ( n=12) with 12 rats in each group by random number table method: Sham group, myocardial ischemia reperfusion group (group I/R), gabapentin group (group Gap), LY294002 group (group LY) and gabapentin +LY294002 group (group Gap +LY). The model of myocardial ischemia reperfusion injury was established by ligation of the left anterior descending coronary artery for 30 min and reperfusion for 120 min. Heart rate (HR), mean arterial pressure (MAP) and the rate pressure product (RPP) were recorded at baseline before ischemia (T 0) for 30 min (T 1) and reperfusion for 120 min (T 2) to evaluate hemodynamic changes during ischemia and reperfusion; The frequency of PVCs and VT/VF were recorded to evaluate the occurrence of arrhythmias during ischemia/reperfusion. TTC staining was used to detect myocardial infarction area. And the protein expression levels of PI3K and Akt in myocardial tissue were detected by Western blotting. Results:Compared with group I/R, the myocardial infarction area, PVCs and VT/VF times, and the protein expression levels of PI3K and p-Akt were significantly increased in group Gap ( P<0.05). Compared with group Gap, the area of myocardial infarction, the number of PVCs and VT/VF, and the protein expression of PI3K and p-Akt were significantly decreased in the group Gap +LY ( P<0.05). Conclusions:Gabapentin can alleviate myocardial ischemia-reperfusion injury, and its mechanism is related to the activation of PI3K-AKT signaling pathway.

Changes of mitochondrial fission and fusion after myocardial injury in cardiac arrest rats / 中华急诊医学杂志

Objective:To investigate the dynamic changes of mitochondrial fission and fusion in the heart of cardiac arrest (CA) rats after return of spontaneous circulation (ROSC), and to explore the role of mitochondrial fission and fusion in the myocardial injury after ROSC.Methods:Healthy male SD rats were randomly random number assigned into the post-resuscitation (PR) 4 h ( n=12), PR 24 h ( n=12), PR 72 h ( n=12), and sham groups ( n=6). The rat CA model was induced by asphyxia, and cardiopulmonary resuscitation (CPR) was performed 6 min after CA. The protein expressions of mitochondrial Drp1, Fis1, Mfn1, and Opa1 were determined by Western blot in each group at 4, 24 and 72 h after ROSC. The mRNA expressions of Drp1, Fis1, Mfn1, and Opa1 were determined by RT-PCR. Myocardial ATP content and mitochondrial respiratory function were measured. The histopathologic changes of myocardial tissue were observed under light microscope. One-way analysis of variance (ANOVA) was use to compare quantitative data, and LSD- t test was used for comparison between groups. Results:Compared with the sham group, the protein and mRNA expressions of Drp1 and Fis1 were increased (all P<0.05) and the protein and mRNA expressions of Mfn1 and Opa1 were decreased (all P<0.05) in the PR 4 h and PR 24 h groups. However, there were no statistical differences in the protein and mRNA expressions of Drp1, Fis1, Mfn1, and Opa1 in the PR 72 h group compared with the sham group (all P>0.05). Compared with the sham group, the levels of ATP content [(4.53±0.76) nmol/g protein vs. (8.57±0.44) nmol/g protein and (5.58±0.58) nmol/g protein vs. (8.57±0.44) nmol/g protein] and mitochondrial respiratory control rate [(2.47±0.38) vs. (3.45±0.32) and (2.97±0.24) vs. (3.45±0.32)] were obviously decreased in the PR 4 h and PR 24 h groups (all P<0.05). There were no statistically significant differences in the ATP content [(7.73±0.95) nmol/g protein vs. (8.57±0.44) nmol/g protein] and mitochondrial respiratory control ratio [(3.39±0.34) vs. (3.45±0.32)] between the PR 72 h group and the sham group (all P>0.05). The pathological damage of myocardial tissue was obvious in the PR 4 h group, and was improved significantly in the PR 72 h group. Conclusions:The imbalance of mitochondrial fission and fusion is probably involved in the pathological process of myocardial injury after ROSC, which may be related to mitochondrial dysfunction.

Effects of acupuncture on the expression of CaMK II mRNA and apoptosis in the myocardial ischemic/reperfused injury rats / 国际中医中药杂志

Objective:To observer the effect of electroacupuncture at "Neiguan", "Ximen" and "Hegu" acupoints of the Pericardium Meridian and observe the expression of CaMK Ⅱ mRNA and apoptosis in the myocardial ischemic rats with reperfused injury.Methods:The Wister rats were randomly divided into sham operation group, model group, Acupuncture Neiguan group, Acupuncture Ximen group and Acupuncture Hegu group, with 10 rats in each group. Exceptthe sham operation group, the othergroups were all ligated with the left anterior descending branch of the coronary artery. Before ligating the coronary artery, electroacupuncture was performed at "Neiguan", "Ximen" and "Hegu" points for 20 minutes respectively. After the ligation for 40 minutes, electroacupuncture was performed at the above points for 20 minutes and then restore coronary perfusion for 60 minutes. The ECG changes of rats were recorded. The level of CaMK Ⅱ mRNA was detected by RT-PCR and the apoptosis rate of cardiomyocytes was detected by TUNEL. The correlation between the expression rate of CaMK Ⅱ mRNA and the apoptosis rate of cardiomyocytes was analyzed according to the pearson correlation.Results:At 20, 40 and 60 min after the ligation of coronary artery and 30 and 60 min after the loosening of coronary artery, compared with the model group and Acupuncture Hegu group, the ST segment difference of Acupuncture Neiguan group and Acupuncture Ximen group was decreased ( P<0.01); The levels of CaMK Ⅱ mRNA (0.483 ± 0.050, 0.432 ± 0.079 vs. 0.935 ± 0.109) in Acupuncture Neiguan group and Acupuncture Ximen group were significantly decreased ( P<0.01). The apoptosis rate of cardiomyocytes (10.86% ± 2.17%, 9.66% ± 4.09% vs. 36.22% ± 1.69%) significantly decreased ( P<0.01). Conclusions:There is a positive correlation between CaMK Ⅱ mRNA level and cardiomyocyte apoptosis during myocardial ischemia-reperfusion. Acupuncture can effectively reduce CaMK Ⅱ mRNA level and cardiomyocyte apoptosis rate and protect cardiomyocytes.

Research advances in targeting autophagy to alleviate hepatic ischemia-reperfusion injury / 临床肝胆病杂志

Hepatic ischemia-reperfusion injury (HIRI) is a common clinical problem after hepatectomy and liver transplantation and is the main cause of liver dysfunction and liver failure after transplantation. In recent years, autophagy-mediated pathways have become a research hotspot in alleviating HIRI. Autophagy refers to the process in which a large number of substrates such as cytoplasm and damaged organelles are transported into lysosomes for digestion and degradation, so as to constantly renew, reshape, and reuse cells. This article summarizes the research advances in the mechanism of targeting autophagy to alleviate HIRI from the aspects of gene, protein, signaling pathway, inflammatory response, oxidative stress, and mitochondrial and endoplasmic reticulum stress, as well as existing problems and prospects in research, in order to provide theoretical support for the future research on alleviating HIRI by targeting autophagy.