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INHIBITORY EFFECT OF TRIMETAZIDINE ON CARDIAC MYOCYTE APOPTOSIS IN RABBIT MODEL OF ISCHEMIA-REPERFUSION 被引量:6
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作者 Rasheed AL-ghazali 《Chinese Medical Sciences Journal》 CAS CSCD 2004年第4期242-242,共1页
关键词 Animals APOPTOSIS Male MALONDIALDEHYDE Myocardial ischemia Myocardial reperfusion Injury Myocytes cardiac Protective Agents Rabbits Random Allocation Research Support Non-U.S. Gov't Superoxide Dismutase TRIMETAZIDINE
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Protective function of tocilizumab in human cardiac myocytes ischemia reperfusion injury 被引量:6
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作者 Hai-Feng Cheng Yan Feng +2 位作者 Da-Ming Jiang Kai-Yu Tao Min-Jian Kong 《Asian Pacific Journal of Tropical Medicine》 SCIE CAS 2015年第1期48-52,共5页
Objective:To investigate the protective function of tocilizumab in human cardiac myocytes ischemia-reperfusion injury.Methods:The human cardiac myocytes were treated by tocilizumab with different concentrations(1.0 mg... Objective:To investigate the protective function of tocilizumab in human cardiac myocytes ischemia-reperfusion injury.Methods:The human cardiac myocytes were treated by tocilizumab with different concentrations(1.0 mg/mL,3.0 mg/mL,5.0 mg/mL) for 24 h.then cells were cultured in ischemia environment for 24 h and reperfusion environment for 1 h.The MTT and flow cytometry were used to detect the proliferation and apoptosis of human cardiac myocytes,respectively.The mRNA and protein expressions of Bcl-2 and Bax were measured by qRT-PCR and western blot,respectively.Results:Compared to the negative group,pretreated by tocilizumab could significantly enhance the proliferation viability and suppress apoptosis of human cardiac myocytes after suffering ischemia reperfusion injury(P<0.05).The expression of Bcl-2 in tocilizumab treated group were higher than NC group(P<0.05).while the Bax expression were lower(P<0.05).Conclusions:Tocilizumab could significantly inhibit apoptosis and keep the proliferation viability of human cardiac myocytes after suffering ischemia reperfusion injury.Tocilizumab may obtain a widely application in the protection of ischemia reperfusion injury. 展开更多
关键词 TOCILIZUMAB HUMAN cardiac MYOCYTES ischemia-reperfusion INJURY Protection
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Tauroursodeoxycholic acid and 4-phenyl butyric acid alleviate endoplasmic reticulum stress and improve prognosis of donation after cardiac death liver transplantation in rats 被引量:8
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作者 Hao Lu Ling Lu +5 位作者 Zhen-Chao Xu Yun-Jie Lu Bo Zhao Lin Zhuang Bao-Bing Hao Feng Zhang 《Hepatobiliary & Pancreatic Diseases International》 SCIE CAS 2014年第6期586-593,共8页
BACKGROUND: Inevitable warm ischemia time before organ procurement aggravates posttransplantation ischemia- reperfusion injury. Endoplasmic reticulum (ER) stress is involved in ischemia-reperfusion injury, but its ... BACKGROUND: Inevitable warm ischemia time before organ procurement aggravates posttransplantation ischemia- reperfusion injury. Endoplasmic reticulum (ER) stress is involved in ischemia-reperfusion injury, but its role in donation after cardiac death (DCD) liver transplantation is not clear and the effect of ER stress inhibitors, tauroursodeoxycholic acid (TUDCA) and 4-phenyl butyric acid (PBA), on the prognosis of recipient of DCD liver transplantation remains unclear. METHODS: Male Sprague-Dawley rats (8-10 weeks) were randomly divided into control group: liver grafts without warm ischemia were implanted; DCD group: warm ischemia time of the liver grafts was 60 minutes; TUDCA and PBA groups: based on the DCD group, donors were intraperitoneally injected with TUDCA or PBA 30 minutes before the organ procurements. Serum aminotransferase levels, oxidative stress activation and expression of ER stress signal molecules were evaluated. Pathological examinations were performed. The survivals of the recipients in each group were compared for 14 days.RESULTS: Compared with the control group, DCD rats had significantly higher levels of serum aminotransferase at 6 hours, 1 day and 3 days after operation (P〈0.01, 0.01 and 0.05, respectively) and oxidative indices (P〈0.01 for both malondialdehyde and 8-hydroxy deoxyguanosine), more severe liver damage (P〈0.01) and up-regulated ER stress signal expressions (P〈0.01 for GRP78, phos-eIF2al, CHOP, ATF-4, ATF-6, PERK, XBP-1 and pro-caspase-12). All recipients died within 3 days after liver transplantation. Administration of TUDCA or PBA significantly decreased aminotransferase levels (P〈0.05), increased superoxide dismutase activities (P〈0.01), alleviated liver damage (P〈0.01), down-regulated ER stress signal expressions (P〈0.01) and improved postoperative survivals (P〈0.01). CONCLUSIONS: ER stress was involved with DCD liver trans- plantation in rats. Preoperative intraperitoneally injection of TUDCA or PBA protected ER stress and improved prognosis. 展开更多
关键词 donation after cardiac death liver transplantation ischemia-reperfusion injury endoplasmic reticulum stress
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A protease-activated receptor 1 antagonist protects against global cerebral ischemia/reperfusion injury after asphyxial cardiac arrest in rabbits 被引量:2
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作者 Jing-ning Yang Jun Chen Min Xiao 《Neural Regeneration Research》 SCIE CAS CSCD 2017年第2期242-249,共8页
Cerebral ischemia/reperfusion injury is partially mediated by thrombin, which causes brain damage through protease-activated receptor 1(PAR1). However, the role and mechanisms underlying the effects of PAR1 activati... Cerebral ischemia/reperfusion injury is partially mediated by thrombin, which causes brain damage through protease-activated receptor 1(PAR1). However, the role and mechanisms underlying the effects of PAR1 activation require further elucidation. Therefore, the present study investigated the effects of the PAR1 antagonist SCH79797 in a rabbit model of global cerebral ischemia induced by cardiac arrest. SCH79797 was intravenously administered 10 minutes after the model was established. Forty-eight hours later, compared with those administered saline, rabbits receiving SCH79797 showed markedly decreased neuronal damage as assessed by serum neuron specific enolase levels and less neurological dysfunction as determined using cerebral performance category scores. Additionally, in the hippocampus, cell apoptosis, polymorphonuclear cell infiltration, and c-Jun levels were decreased, whereas extracellular signal-regulated kinase phosphorylation levels were increased. All of these changes were inhibited by the intravenous administration of the phosphoinositide 3-kinase/Akt pathway inhibitor LY29004(3 mg/kg) 10 minutes before the SCH79797 intervention. These findings suggest that SCH79797 mitigates brain injury via anti-inflammatory and anti-apoptotic effects, possibly by modulating the extracellular signal-regulated kinase, c-Jun N-terminal kinase/c-Jun and phosphoinositide 3-kinase/Akt pathways. 展开更多
关键词 nerve regeneration protease-activated receptor 1 global cerebral ischemia/reperfusion cardiac arrest neuroprotection SCH79797 apoptosis inflammation neuron specific enolase hippocampus neural regeneration
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Allograft Inflammatory Factor-1 in Cardiac Ischemia Re-perfusion Injury: Release of Molecular Markers in an <i>in Vitro</i>Setting
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作者 D. Olga McDaniel Xinchun Zhou +5 位作者 Debbie A. Rigney Larry S. McDaniel Giorgio Aru Curtis Tribble Lawrence Creswell Walter H. Merrill 《Open Journal of Organ Transplant Surgery》 2013年第1期5-12,共8页
Initial ischemia/reperfusion injury (IRI) may have an impact on recipient immune responses after transplantation. Allograft inflammatory factor-1 (AIF-1) has been implicated in the regulation of inflammation associate... Initial ischemia/reperfusion injury (IRI) may have an impact on recipient immune responses after transplantation. Allograft inflammatory factor-1 (AIF-1) has been implicated in the regulation of inflammation associated with organ rejection. We hypothesized that it is either passively released from injured tissues during organ procurement, or actively secreted by allograft infiltrating cells contributing to allograft dysfunction. We investigated the impact of IRI in an in vitro study of human heart tissue during the process of transplantation. The mRNA expression levels for both isoforms of the AIF-1, I2 and I3 were significantly increased after 30 minutes reperfusion (AIF-1 I2: p 0.01 vs. AIF-1 I3: p 0.005). Expression levels for IL-18 and the TLRs were increased after 30 minutes of reperfusion. Only IL-18 and TLR-2 were statistically significant (IL-18: p 0.0001 vs. TLR-2: p 0.01). The mRNA expression levels for AIF-1 I2 and IL-18 were decreased from the original levels of ischemia after 60 and 90 minutes reperfusion. The TLR-2 and -4 were presented with minimal levels of reduction after 60 minutes. However, mRNA expression levels for all were decreased to the original levels of ischemia after 90 minutes, except for AIF-1 I3, but the difference was not statistically significant. AIF-1 and IL-18 were specifically detected in myocytes and interstitial tissues by immunohistochemistry (IHC) stain after IRI. TLR-4 was non-specific, and TLR2 was minimally expressed. The study discusses the evidence supporting that the AIF-1 may have therapeutic potential for strategies in the control of innate immune responses early on, after transplantation. 展开更多
关键词 ALLOGRAFT Inflammatory Factor-1 cardiac MYOCYTES Innate Immunity ischemia/reperfusion Rejection TOLL-LIKE Receptors
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Cardio-Protective Effects of Oral Nicorandil in Patients Undergoing Cardiac Valve Surgery
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作者 Mohamed A. W. Ezzat Essam Elbadry Hashim Mohamed +3 位作者 Ayman Mohamed Abdel Ghaffar Abdelhady Ahmed Helmy Wesam Abdelgalil Aboelwafa Eman Mohammad Ali 《World Journal of Cardiovascular Diseases》 2019年第10期707-717,共11页
Background: Reduction of myocardial reperfusion injury during cardiopulmonary bypass is an essential requirement for increasing the success rate, decreasing morbidity and mortality of open-heart surgery. Aim: To study... Background: Reduction of myocardial reperfusion injury during cardiopulmonary bypass is an essential requirement for increasing the success rate, decreasing morbidity and mortality of open-heart surgery. Aim: To study the role of pre-operative oral nicorandil in decreasing reperfusion cardiac injury in patients subjected to cardiac valve surgery. Patients and Methods: The study included 62 patients, who were equally randomized into two groups: nicorandil group and control group. Pre-operative, intra-operative and post- operative data were reported and analyzed. Left Ventricle Ejection Fraction (LVEF) was estimated pre-operatively and postoperatively for both groups. Troponin I, creatine kinase-muscle/brain (CK-MB), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) were measured before surgery by 24 hours then 4, 12 and 48 hours after aortic cross clamp removal. Results: Nicorandil considerably decreased TNF-α and IL-6 after 4 and 12 hours following the removal of aortic clamping. It also reduced troponin-I and CKMB at the same time points. However, there were no important changes in IL-6, TNF-α, troponin-I and CK-MB levels in control group in comparison to nicorandil group in the next 48 hours following the removal of aortic clamping. Conclusions: Pre-operative oral nicorandil expressively decreased myocardial reperfusion damage during open heart valve operations, this evidenced by the decrease in the postoperative use of inotropic drugs, considerable reduction of postoperative elevation of cardiac enzymes and inflammatory cytokines with no reported complications. 展开更多
关键词 NICORandIL for Myocardial Protection CARDIOPULMONARY BYPASS ischemia-reperfusion Injury Inflammatory Cytokines cardiac Valvular Surgery
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INCREASED VULNERABILITY OF HYPERTROPHIED MYOCARDIUM TO ISCHEMIA AND REPERFUSION INJURY RELATION TO CARDIAC RENIN-ANGIOTENSIN SYSTEM 被引量:1
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作者 章友华 徐守春 《Chinese Medical Journal》 SCIE CAS CSCD 1995年第1期28-32,共5页
Hearts of pressure-overload hypertrophy show an increased activation of intracardiac renin-angiotensin system which may contribute to ischemia and reperfusion injury. The purpose of this study is to evaluate whether t... Hearts of pressure-overload hypertrophy show an increased activation of intracardiac renin-angiotensin system which may contribute to ischemia and reperfusion injury. The purpose of this study is to evaluate whether the hypertrophied myocardium is more vulnerable to ischemia and reperfusion injury and to find out its relation to the cardiac renin-angiotensin system. Hypertrophied rat hearts induced by abdominal aortic banding for 6 weeks were subjected to 2 hours of hypothermic ischemic arrest followed by 30 minutes of reperfusion, and their cardiac function recovery was compared with that of sham-operated normal control hearts. The cardiac renin activity and angiotensin II content before ischemia and after reperfusion were determined. It was found that both the pre-ischemic renin activity and angiotensin II level were higher in hypertrophied myocardium than those in the control: ischemia and reperfusion injury increased both renin activity and angiotensin II content in the two groups, but the renin activity and angiotensin II level were further elevated after reperfusion in the hypertrophied hearts than those in the control hearts. Meanwhile, the cardiac function recovery after 30 minutes reperfusion in the hypertrophied hearts was poorer than that in the control. Correlation analysis revealed that there was a negative correlation between the cardiac output recovery and the myocardial angiotensin II content (r=-0.841), P<0.001), It is concluded that ischemia and reperfusion injury can activate cardiac renin-angiotensin system in isolated rat heart, which may be responsible for the increased susceptibility of the hypertrophied myocardium to ischemia and reperfusion injury. 展开更多
关键词 LVEDP INCREASED VULNERABILITY of HYPERTROPHIED MYOCARDIUM TO ischemia and reperfusion INJURY RELATION TO cardiac RENIN-ANGIOTENSIN SYSTEM LVSP In mode than
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Antioxidant properties of magnesium lithospermate B contribute to the cardioprotection against myocardial ischemia/reperfusion injury in vivo and in vitro 被引量:23
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作者 Wei Quan Ying Yin +7 位作者 Miaomiao Xi Dan Zhou Yanrong Zhu Yue Guan Chao Guo Yanhua Wang Jialin Duan Aidong Wen 《Journal of Traditional Chinese Medicine》 SCIE CAS CSCD 2013年第1期85-91,共7页
OBJECTIVE: To determine the cardioprotective ef- fect of magnesium lithospermate B (MLB) on myo- cardial ischemia/reperfusion (MI/R) injury and to in- vestigate the antioxidant potential in vivo and in vitro. MET... OBJECTIVE: To determine the cardioprotective ef- fect of magnesium lithospermate B (MLB) on myo- cardial ischemia/reperfusion (MI/R) injury and to in- vestigate the antioxidant potential in vivo and in vitro. METHODS: MI/R injury was induced by the occlu- sion of left anterior descending coronary artery for 30 min followed by reperfusion for 3 h in rats. After reperfusion, hearts were harvested to assess infarct size, histopathological damages, the levels of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), reduced glutathione (GSH) and malondialdehyde (MDA). Blood samples were collected to determine serum levels of creatine kinase-MB (CK-MB), cardiac troponin (cTnl) and lactate dehydrogenase (LDH). Furthermore, simulatedischemia/reperfusion (SI/R) injury in vitro was established by oxygen and glucose deprivation (OGD) for 2 h followed by 24-hour recovery period in cardiomyocytes. The activity of LDH in the cultured su- pernatant and the levels of intracellular reactive oxygen species (ROS), SOD and MDA in cardiomyo- cytes were also measured. Finally, cardiomyocytes apoptosis was determined with flow cytometry. RESULTS: MLB significantly limited infarct size, ameliorated histopathological damages and prevented leakage of CK-MB, cTnl and LDH. Additional- ly, SOD, CAT, GPx and GSH activities were notably increased by MLB, along with the MDA content decreased as compared with the model group in rats. In vitro study, MLB also decreased LDH activity in the cultured supernatant, increased SOD activity in cardiomyocytes, reduced intracellular ROS and MDA levels, and significantly suppressed cardiomyocytes apoptosis. CONCLUSION: MLB possessed remarkably cardioprotective effects on MI/R injury in vivo and in vitro. The protection of MLB may contribute to its antioxidant properties. 展开更多
关键词 ischemia reperfusion injury Myocytes cardiac Oxidative stress ANTIOXIDANTS In vitro Magnesium lithospermate B
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Mild hypothermia in improving multiple organ dysfunction after cardiac arrest 被引量:7
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作者 LinYang Xu-ming Zhao Li-junLiu 《World Journal of Emergency Medicine》 SCIE CAS 2010年第3期196-200,共5页
BACKGROUND: Resuscitation after cardiac arrest (CA) with a whole-body ischemia–reperfusion injury causes brain injury and multiple organ dysfunction (MODS). This study aimed to determine whether mild systemic hy... BACKGROUND: Resuscitation after cardiac arrest (CA) with a whole-body ischemia–reperfusion injury causes brain injury and multiple organ dysfunction (MODS). This study aimed to determine whether mild systemic hypothermia could decrease multiple organ dysfunctions after resuscitation from cardiac arrest.METHODS: The patients who had been resuscitated after cardiac arrest were reviewed. During the resuscitation they had been assigned to undergo therapeutic hypothermia (target temperature, 32°C to 34°C, measured in the rectum) over a period of 24 to 36 hours or to receive standard treatment with normothermia. Markers of different organ injury were evaluated for the ? rst 72 hours after recovery of spontaneous circulation (ROSC).RESULTS: At 72 hours after ROSC, 23 patients in the hypothermia group for whom data were available had favorable neurologic, myocardial, hepatic and pulmonic outcomes as compared with 26 patients in the normothermia group. The values of renal function were not signi? cantly different between the two groups. However, blood coagulation function was badly injured in the hypothermia group.CONCLUSION: In the patients who have been successfully resuscitated after cardiac arrest, therapeutic mild hypothermia can alleviate dysfunction after resuscitation from cardiac arrest. 展开更多
关键词 cardiac arrest ischemia reperfusion injury Mild hypothermia Multiple organ dysfunction
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ACIDIC FIBROBLAST GROWTH FACTOR REDUCES RAT SKELETAL MUSCLE DAMAGE CAUSED BY ISCHEMIA AND REPERFUSION 被引量:6
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作者 傅小兵 Cuevas P. +2 位作者 Gimenez-Gallego G 盛志勇 田惠民 《Chinese Medical Journal》 SCIE CAS CSCD 1995年第3期51-56,共6页
Acute interruption of arterial blood flow to the extremities is often associated with significant morbidity and mortality. Broad spectrum mitogenic and non mitogenic activities of FGFs inspired us to study its protect... Acute interruption of arterial blood flow to the extremities is often associated with significant morbidity and mortality. Broad spectrum mitogenic and non mitogenic activities of FGFs inspired us to study its protecting effects on tissue injuries in ischemia reperfusion condition. We found that systemic administration of aFGF after reperfusion onset prevented severe skeletal muscle injuries. In rats treated with aKGF, the tissue edema was reduced significantly, the tissue viability was increased, and the muscle fibers contained more succinate dehydrogenase (SDH) and adenosine triphosphatasc (ATPase). The pathological results supported the concept of improved prevention with aFGF treatment. The possible tissue protection by aFGF may come from its ability to regulate the concentration of evtra- and intracellular calcium ion. Besides, it may moderate other Ca2+ dependent enzyme conversion processes. Also, it may take part in the vascular tone regulation under ischemia and reperfusion conditions. These results suggest further study of tissue ischemia prevention with FGF and its possible mechanisms in the future. 展开更多
关键词 AFGF ACIDIC FIBROBLAST GROWTH FACTOR REDUCES RAT SKELETAL muscle DAMAGE CAUSED BY ischemia and reperfusion
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Beneficial effects of intermittent hypobaric hypoxia on the body 被引量:9
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作者 Yi ZHANG Zhao-nian ZHOU 《中国应用生理学杂志》 CAS CSCD 2012年第6期504-509,共6页
Myocardial ischemia and reperfusion(I/R) is a common problem in clinic and there is no satisfactory method for prevention or treatment of I/R injury so far.Chronic intermittent hypobaric hypoxia(CIHH),similar to the c... Myocardial ischemia and reperfusion(I/R) is a common problem in clinic and there is no satisfactory method for prevention or treatment of I/R injury so far.Chronic intermittent hypobaric hypoxia(CIHH),similar to the concept of ischemia preconditioning(IPC)or altitude hypoxia adaptation(AHA),has been recognized to confer a protective effect on heart against I/R injury with a longer protective effect than IPC and a less adverse effect than AHA.It has been proved that CIHH increases myocardial tolerance to ischemia or hypoxia,reserving cardiac function and preventing arrhythmia during I/R.Multiple mechanisms or pathway underlying the cardiac protection of CIHH have been proposed,such as induction of heatshock protein,enhancement of myocardial antioxidation capacity,increase of coronary flow and myocardial capillary angiogenesis,activation of adenosine triphosphate(ATP)-sensitive potassium channels,inhibition of mitochondrial permeability transition pores,and activation of protein kinase C(PKC) and induced nitric oxide synthase(iNOS).In addition,CIHH has been found having many beneficial effects on the body,such as promotion of health,increase of oxygen utilization,and prevention or treatment for some diseases.The beneficial effects of CIHH and potential mechanisms are reviewed mainly based on the researches performed by our group. 展开更多
关键词 低氧适应 间歇性 有益作用 诱导型一氧化氮合酶 心肌缺血再灌注 低压 保护作用 心脏功能
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Myocardial Protection during Cardiac Surgery: Warm Blood versus Crystalloid Cardioplegia
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作者 Helene De Bruyn France Gelders +8 位作者 Tine Gregoir Valerie Waelbers Pascal Starinieri Jean-Louis Pauwels Jeroen Lehaen Boris Robic Alaaddin Yilmaz Urbain Mees Marc Hendrikx 《World Journal of Cardiovascular Diseases》 2014年第9期422-431,共10页
Purpose: Prevention of myocardial injury is essential during cardiac surgery. Both crystalloid and blood cardioplegia are popular methods for myocardial protection. Most experimental studies have been in favor of bloo... Purpose: Prevention of myocardial injury is essential during cardiac surgery. Both crystalloid and blood cardioplegia are popular methods for myocardial protection. Most experimental studies have been in favor of blood cardioplegia. The objective of this study is to determine whether the use of warm blood cardioplegia (BCP) is superior to crystalloid cardioplegia (CCP) by means of myocardial injury markers and clinical outcome parameters. Materials and Methods: In a consecutive series of 293 patients, the first 150 received crystalloid cardioplegia, whereas the next 143 patients received blood cardioplegia. Postoperative myocardial injury was assessed by CTnI and CK-MB. Perioperative morbidity and mortality and clinical outcome parameters (need for inotropic support, ICU and hospital stay) were recorded. An unpaired student t-test was performed to analyse continuous postoperative variables relating to myocardial damage. The presence of possible confounders influencing the CTnI or CK-MB concentrations was tested using a student t-test for continuous variables, for categorical variables ANOVA was used. A final longitudinal model was created for CTnI and CK-MB. CTnI was analyzed by a mixed model with random intercept and slope. For all tests performed, statistical significance was 5%. Results: Both groups were well matched with respect to preoperative variables. No significant difference could be found in maximum postoperative levels of CTnI (8.8 ± 18.4 μg/l in BCP vs 9.6 ± 16.5 μg/l in CCP, p = 0.6455) or CK-MB (19.2 ± 31.0 μg/l in BCP vs 26.4 ± 41.5 μg/l in CCP, p = 0.1209). Nor was there any significant difference in other postoperative variables. Testing treatment effect over time proved only significant influence of the surgical intervention type on CTnI levels in time (p < 0.001). Conclusion: This study could not show significantly higher myocardial injury in the group of patients receiving crystalloid cardioplegia versus warm blood cardioplegia. This suggests that warm blood cardioplegia does not confer superior myocardial protection. Surgical intervention type has an important effect on CTnI concentration in time, while the type of cardioplegia does not. 展开更多
关键词 MYOCARDIUM Protection ischemia/reperfusion MYOCARDIAL INFARCTION cardiac Surgery
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Physical Training and Cardioprotection
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作者 Keith L.March 《中国运动医学杂志》 CAS CSCD 北大核心 2003年第4期378-382,共5页
Experimental, clinical and epidemiologic studies have provided strong evidence that physical training has beneficial effects on cardiovascular health. Numerous investigations have demonstrated that exercise increases ... Experimental, clinical and epidemiologic studies have provided strong evidence that physical training has beneficial effects on cardiovascular health. Numerous investigations have demonstrated that exercise increases coronary blood flow and myocardial perfusion. Importantly, training also can stimulate angiogenesis and accelerate collateral vessel growth in animal models with coronary artery occlusion. Cardiac adaptation such as increased vascularity or capillary density has been evidenced after regular endurance exercises. More recently, several studies indicate that physical training induces high levels of myocardial heat shock protein and antioxidant protein expression, which may play an important role in myocardial protection against ischemia-reperfusion injury. 展开更多
关键词 心脏保护 体育疗法 血管生成 心肌缺血再灌注损伤
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重楼皂苷Ⅰ预防给药对心肌缺血再灌注损伤大鼠调节PI3K/AKT信号通路的作用研究
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作者 田俊斌 赵静 +2 位作者 罗斌 吕建瑞 马磊 《西部医学》 2024年第3期317-324,共8页
目的 从磷脂酰肌醇-3-激酶(PI3K)/蛋白激酶B(AKT)信号通路探讨重楼皂苷I预防给药对心肌缺血再灌注损伤(MI/IR)大鼠的干预机制。方法 将购买的72只SPF级SD大鼠按照随机数字法分为假手术组、模型组、阿司匹林组、重楼皂苷I低、中和高剂量... 目的 从磷脂酰肌醇-3-激酶(PI3K)/蛋白激酶B(AKT)信号通路探讨重楼皂苷I预防给药对心肌缺血再灌注损伤(MI/IR)大鼠的干预机制。方法 将购买的72只SPF级SD大鼠按照随机数字法分为假手术组、模型组、阿司匹林组、重楼皂苷I低、中和高剂量组,每组12只。分组后即给予相应药物干预2周,2周后构建MI/IR模型。模型构建成功24 h后先采用动物彩色多普勒超声仪检测心脏功能,后处死大鼠收集相关组织采用HE染色观察心肌病理学、TTC法检测心肌梗死面积,试剂盒检测心功能指标[乳酸脱氢酶(LDH)、肌酸激酶同工酶MB(CK-MB)和谷草转氨酶(AST),抗氧化指标丙二醛(MDA)、超氧化物歧化酶(SOD)和谷胱甘肽(GSH)],TUNNEL染色检测心肌细胞凋亡特点,Western blot检测心肌PI3K、AKT、B细胞淋巴瘤/因子2(Bcl-2)、Bcl-2相关蛋白(Bax)蛋白表达。结果 假手术组心肌纤维排列整齐、无水肿,模型组有心肌纤维断裂,重楼皂苷I低、中、高剂量组和阿司匹林组明显改善心肌纤维断裂情况。与假手术组相比,模型组大鼠心肌梗死面积、LVEDP、LDH、CK-MB、AST和MDA明显升高(P<0.05),LVDP、+dp/dtmax、-dp/dtmax、SOD和GSH明显降低(P<0.05);相较于模型组,阿司匹林组和重楼皂苷I低、中、高剂量组干预后,心肌梗死面积、LVEDP、LDH、CK-MB、AST和MDA明显降低(P<0.05),LVDP、+dp/dtmax、-dp/dtmax、SOD和GSH则明显升高(P<0.05)。Tunnel染色可见,假手术组几乎没有心肌细胞凋亡,而模型组呈现出明显的大量的细胞凋亡;与模型组相比,阿司匹林组和重楼皂苷I低、中、高剂量组凋亡情况明显好转。此外,与假手术组相比,模型组大鼠心肌PI3K、AKT和Bcl-2蛋白表达均明显降低,Bax明显升高(均P<0.05);相较于模型组,重楼皂苷I低、中、高剂量组以及阿司匹林组PI3K、AKT和Bcl-2蛋白表达均明显升高,Bax蛋白表达明显降低(均P<0.05)。结论 重楼皂苷I对心肌缺血再灌注损伤有一定的预防作用,其作用机理可能与其能够调节PI3K/AKT信号通路有关。 展开更多
关键词 重楼皂苷I 心肌缺血再灌注损伤 PI3K/AKT信号通路 心功能
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肌醇需求酶1信号通路在自噬改善大鼠冠心病心肌缺血损伤中的作用
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作者 尹磊 王剑 +2 位作者 金静 章若涵 刘燕飞 《中国循环杂志》 CSCD 北大核心 2024年第5期503-510,共8页
目的:基于探讨肌醇需求酶1(IRE1)信号通路在自噬改善大鼠冠心病心肌缺血损伤中的作用。方法:将H9c2细胞分为对照组、IRE1组、缺氧缺糖(OGD)/复氧(OGD/R)组、OGD/R+IRE1组、氯喹组、IRE1+氯喹组、OGD/R+氯喹组、OGD/R+IRE1+氯喹组、OGD组... 目的:基于探讨肌醇需求酶1(IRE1)信号通路在自噬改善大鼠冠心病心肌缺血损伤中的作用。方法:将H9c2细胞分为对照组、IRE1组、缺氧缺糖(OGD)/复氧(OGD/R)组、OGD/R+IRE1组、氯喹组、IRE1+氯喹组、OGD/R+氯喹组、OGD/R+IRE1+氯喹组、OGD组、OGD+氯喹组、OGD/R+IRE1+敲低X盒结合蛋白1(si-XBP1)组、OGD/R+IRE1+过表达X盒结合蛋白1(XBP1-OE)组。通过自噬双标腺病毒(Adv-RFP-GFP-LC3)评估各组细胞的自噬通量。通过免疫荧光和免疫印迹分析X盒结合蛋白1(XBP1)的核转位。另将32只成年雄性C57BL/6 J小鼠随机分为假手术组、缺血/再灌注(I/R)组、IRE1组和I/R+IRE1组,每组8只。通过超声心动图评估大鼠心功能。通过定量免疫印迹分析自噬相关蛋白。结果:(1)细胞试验:与OGD/R组比,OGD/R+IRE1组H9c2细胞中IRE1蛋白表达水平显著增加(P<0.001),微管相关蛋白轻链3蛋白Ⅱ(LC3Ⅱ)和泛素结合蛋白(p62)蛋白表达均显著降低(P均<0.05)。与OGD/R+氯喹组比,OGD/R+IRE1+氯喹组H9c2细胞中LC3Ⅱ和p62蛋白表达均显著增加(P均<0.05)。与对照组比,OGD/R组H9c2细胞中IRE1细胞核/细胞质荧光强度比显著增加(P<0.001);与OGD/R组比,OGD/R+IRE1组IRE1细胞核/细胞质荧光强度增加(P<0.001)。与OGD/R组比,OGD/R+IRE1组核蛋白中的XBP1水平增加(P<0.05)。与OGD/R+IRE1组比,OGD/R+IRE1+si-XBP1组黄色点状体显著减少(P<0.01),OGD/R+IRE1+XBP1-OE组黄色点状体显著增加(P<0.05)。(2)大鼠体内实验:与假手术组比,I/R组左心室射血分数和短轴缩短率均显著降低(P均<0.05)。与I/R组比,I/R+IRE1组心功能障碍改善(P均<0.05)。与假手术组比,I/R组心肌自噬空泡的数量、IRE1、LC3Ⅱ和p62表达均显著增加(P均<0.05)。与I/R组比,I/R+IRE1组心肌自噬空泡的数量、p62表达均显著降低(P均<0.05),心肌组织中IRE1、LC3Ⅱ的表达均增加(P均<0.05)。结论:IRE1通过促进XBP1的核转位恢复了OGD/R和I/R诱导的自噬通量阻断,自噬通量的恢复有助于保护心功能。 展开更多
关键词 肌醇需求酶1 心功能 心肌缺血/再灌注 缺氧缺糖/复氧 自噬通量
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缺血后处理对心肌缺血再灌注大鼠心功能、心肌细胞凋亡和心肌组织线粒体凋亡相关分子表达的影响
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作者 王涛 郝恩刚 《医学分子生物学杂志》 CAS 2024年第6期586-590,596,共6页
目的分析缺血后处理(ischemic postconditioning,IP)对心肌缺血再灌注(ischemia-reperfusion,IR)大鼠心功能、心肌细胞凋亡和心肌组织线粒体凋亡相关分子表达的影响。方法将40只8周龄雄性SD大鼠分笼喂养,每笼5只,适应性饲养7 d,随机分... 目的分析缺血后处理(ischemic postconditioning,IP)对心肌缺血再灌注(ischemia-reperfusion,IR)大鼠心功能、心肌细胞凋亡和心肌组织线粒体凋亡相关分子表达的影响。方法将40只8周龄雄性SD大鼠分笼喂养,每笼5只,适应性饲养7 d,随机分为空白对照组(对照组)、假手术组(S组)、心肌IR造模组(IR组)、心肌IP造模+IP处理组(IP组),每组各10只。术后4 h使用生物机能实验系统记录大鼠心功能[左心室收缩压(left ventricular systolic pressure,LVSP)、心室舒张末压(left ventricular enddiastolic pressure,LVEDP)、左心室压变化速率最大值(±dp/dtmax)]。采用TUNEL法检测心肌细胞凋亡指数,采用RT-PCR法检测心肌细胞凋亡相关蛋白BCL-2、BAX及天冬氨酸特异性半胱氨酸蛋白酶-3(cysteinylaspartate-specific proteinase 3,Caspase-3)、法尼酯衍生物X受体(farnesyl X receptor,FXR)、小异二聚体配体(small heterodimer partner,SHP)相对表达量。蛋白质印迹法检测心肌细胞线粒体凋亡通路标志物细胞色素C(cytochrome C,Cyt-C)的释放量。结果IP组及IR组LVEDP、心肌细胞凋亡指数、心肌组织BAX、CASPASE-3、FXR、SHP相对表达量及心肌细胞胞浆Cyt-C蛋白灰度值均高于S组、对照组(P<0.05),IR组LVEDP、心肌细胞凋亡指数、BAX、CASPASE-3、FXR、SHP相对表达量及Cyt-C蛋白灰度值高于IP组(P<0.05);IP组及IR组LVSP、±dp/dtmax、心肌组织BCL-2相对表达量均低于S组、对照组(P<0.05),IR组LVSP、±dp/dtmax、心肌组织BCL-2相对表达量均低于IP组(P<0.05)。结论IP处理可减轻大鼠心肌IR损伤,改善心功能,可能与调控BCL-2/BAX、FXR/SHP等凋亡相关信号蛋白的表达有关。 展开更多
关键词 心肌缺血再灌注 缺血后处理 心肌细胞凋亡 心肌细胞线粒体凋亡 心功能
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心搏骤停后综合征的治疗方法研究进展 被引量:1
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作者 朱擎天 张鹏飞 +3 位作者 余虹 陈佳瑜 陈斌(综述) 李芳(审校) 《海南医学》 CAS 2024年第10期1509-1514,共6页
心搏骤停后综合征(PCAS)是心搏骤停的严重并发症,致死、致残率极高。如何采用及时有效的治疗措施提高PCAS患者的救治成功率已成为急诊医学界关注和研究的热点问题之一。目前,PCAS的治疗措施主要包括呼吸支持、循环支持、脑保护、冠状动... 心搏骤停后综合征(PCAS)是心搏骤停的严重并发症,致死、致残率极高。如何采用及时有效的治疗措施提高PCAS患者的救治成功率已成为急诊医学界关注和研究的热点问题之一。目前,PCAS的治疗措施主要包括呼吸支持、循环支持、脑保护、冠状动脉血运重建等。本文对当前PCAS的主要治疗方法进行总述,以期为临床医生救治此类患者和开展进一步的研究提供参考。 展开更多
关键词 心搏骤停 心搏骤停后综合征 缺血再灌注损伤 治疗 进展
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全膝关节置换中的缺血再灌注损伤
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作者 杨毅峰 黄健 +1 位作者 叶楠 王琳 《中国组织工程研究》 CAS 北大核心 2024年第6期955-960,共6页
背景:以往针对缺血再灌注损伤的相关机制、表现、防治已有报道。但对全膝关节置换引起的下肢骨骼肌缺血再灌注损伤研究较少,此文重点对全膝关节置换引起下肢缺血再灌注损伤的发病机制、临床影响及防治方法进行综述。目的:通过对全膝关... 背景:以往针对缺血再灌注损伤的相关机制、表现、防治已有报道。但对全膝关节置换引起的下肢骨骼肌缺血再灌注损伤研究较少,此文重点对全膝关节置换引起下肢缺血再灌注损伤的发病机制、临床影响及防治方法进行综述。目的:通过对全膝关节置换引起下肢缺血再灌注损伤的相关文献进行归纳总结,分析其机制、意义,为进一步研究骨骼肌缺血再灌注损伤给出提示。方法:应用计算机检索PubMed数据库、CNKI、万方数据库及维普数据库2000-01-01/2022-04-30发表的相关文章,英文检索词为“ischemia-reperfusion injury,total knee arthroplasty,tourniquet,mechanism,pathophysiology,skeletal muscle,treatment”;中文检索词为“缺血再灌注损伤,全膝人工关节置换术,止血带,机制,病理生理,骨骼肌,治疗”。排除重复性研究及部分相关性较低的基础类文章。最终纳入68篇文献进行综述。结果与结论:(1)缺血再灌注损伤的发病机制与氧自由基、细胞内钙超载、中性粒细胞活化相关,还和高浓度一氧化氮、无复流现象以及细胞凋亡等机制相关,更详尽的机制研究能为将来的防治提供依据;(2)下肢缺血再灌注损伤会造成局部骨骼肌损伤,这可能由手术本身的创伤引起,也可能是缺血再灌注损伤的作用,还需要更有针对性的研究区别二者关系;(3)下肢缺血再灌注损伤甚至会影响远端器官,造成肾脏、肺脏损伤,还会影响局部及全身循环;(4)明确缺血再灌注损伤的影响能为将来的防治指明方向,目前的防治措施主要包括缺血预处理,麻醉药物、抗氧化剂等药物预防;(5)针对全膝关节置换手术引起的下肢骨骼肌缺血再灌注损伤的详细综述,能为将来的诊疗决策提供依据。 展开更多
关键词 缺血再灌注损伤 全膝关节置换 止血带 机制 病理生理 骨骼肌 治疗
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聚吡咯-壳聚糖导电复合水凝胶促进缺血-再灌注损伤后心脏功能的恢复
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作者 王馨竹 王琦 +1 位作者 郎丽敏 何生 《中国组织工程研究》 CAS 北大核心 2024年第15期2315-2322,共8页
背景:导电生物材料被认为是传输心肌修复电信号的潜在候选者,将基于细胞或无细胞的策略与导电生物材料相结合以补充心肌细胞和/或恢复电信号通路,成为一种有前途的心脏修复方法。目的:评估聚吡咯-壳聚糖导电复合水凝胶对心肌缺血-再灌... 背景:导电生物材料被认为是传输心肌修复电信号的潜在候选者,将基于细胞或无细胞的策略与导电生物材料相结合以补充心肌细胞和/或恢复电信号通路,成为一种有前途的心脏修复方法。目的:评估聚吡咯-壳聚糖导电复合水凝胶对心肌缺血-再灌注损伤大鼠心功能的改善作用。方法:采用化学氧化聚合法制备聚吡咯-壳聚糖导电复合水凝胶,表征水凝胶的微观形貌、生物相容性与导电性。取30只成年SD大鼠,利用夹闭心脏左前降支后再松解的方法建立心肌缺血-再灌注损伤模型,造模21 d后,采用随机数字表法将大鼠分为3组:空白组向左心室梗死区及梗死边缘区内注射生理盐水,普通水凝胶组向左心室梗死区及梗死边缘区内注射壳聚糖水凝胶,导电水凝胶组向左心室梗死区及梗死边缘区内注射聚吡咯-壳聚糖导电复合水凝胶,每组10只。设置造模后对应的时间点,分别进行心脏机械功能(超声心动图、压力-体积分析)、心脏电生理(心电图、程序性电刺激、光学映射技术、微电极阵列技术评估、八导联心电图、瘢痕区电阻率)及心脏组织学检测。结果与结论:①导电复合水凝胶表面存在大量孔隙,导电率为(3.19±0.03)×10^(-3)mS/cm,与平滑肌细胞共培养具有良好的生物相容性。②造模后105 d的超声心动图与压力-体积分析检测显示,与空白组、普通水凝胶组比较,导电复合水凝胶可明显改善心肌缺血-再灌注损伤大鼠心脏的收缩功能。造模后105 d的心电图、程序性电刺激、光学映射技术、微电极阵列技术评估、八导联心电图、瘢痕区电阻率检查结果显示,与空白组、普通水凝胶组比较,导电复合水凝胶可明显改善心肌缺血-再灌注损伤大鼠心脏的电传导功能,降低心律失常的发生。造模后105 d的心脏组织Masson染色显示,3组大鼠心肌梗死区均出现不同程度的纤维化,与生理盐水组和普通水凝胶组相比,导电水凝胶组梗死区正常心肌组织较多、纤维化程度较小。③结果表明,聚吡咯-壳聚糖导电复合水凝胶可能通过提高梗死瘢痕区组织电传导速度、增加瘢痕厚度、增强心脏同步收缩、减少受损组织来促进缺血-再灌注损伤后梗死心肌的修复。 展开更多
关键词 导电生物材料 聚吡咯 壳聚糖 水凝胶 缺血-再灌注损伤 心脏组织工程
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HSP70、DLAT、FDX1铜死亡相关蛋白在心肌缺血再灌注损伤中的表达及意义
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作者 姬瑶璇 金雪淼 +3 位作者 王一帆 孙潇 张怀瑢 朱力 《宁夏医科大学学报》 2024年第11期1109-1115,共7页
目的探究铜死亡相关基因热休克蛋白70(HSP70)、硫辛酸化二氢脂酰胺s-乙酰转移酶(DLAT)、铁氧化还原蛋白1(FDX1)在心肌缺血再灌注(I/R)大鼠心肌细胞中的表达情况。方法采用冠状动脉左前降支结扎法,构建大鼠心肌I/R模型。并将40只SPF级雄... 目的探究铜死亡相关基因热休克蛋白70(HSP70)、硫辛酸化二氢脂酰胺s-乙酰转移酶(DLAT)、铁氧化还原蛋白1(FDX1)在心肌缺血再灌注(I/R)大鼠心肌细胞中的表达情况。方法采用冠状动脉左前降支结扎法,构建大鼠心肌I/R模型。并将40只SPF级雄性大鼠完全随机分为4组:第1周模型组(Model组)、第1周假手术组(Sham组)、第4周模型组(Model’组)、第4周假手术组(Sham’组)。分别在造模成功后第1周与第4周对各组大鼠进行心脏磁共振检查,检测心功能指标。采用HE和Masson染色观察心肌组织病理学变化。采用Western blot和RT-qPCR检测心肌组织中HSP70、DLAT、FDX1蛋白及mRNA表达。结果第1周时,Model组大鼠较Sham组大鼠的心肌组织病理损伤严重,心功能降低,心肌组织中HSP70、DLAT、FDX1蛋白及mRNA表达水平升高(P均<0.05)。第4周时,Model’组大鼠较Sham’组大鼠的心肌组织病理损伤严重,心功能进一步降低,心肌组织中HSP70、DLAT、FDX1蛋白及mRNA表达水平升高(P<0.05)。结论铜死亡通过上调心肌细胞HSP70、DLAT、FDX1蛋白在心肌I/R损伤的发病机制中发挥作用。 展开更多
关键词 心肌缺血再灌注损伤 心功能 铜死亡
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