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| 1 | Recent advances in the diagnosis and treatment of acute myocardial infarction显示文摘The Third Universal Definition of Myocardial Infarction(MI) requires cardiac myocyte necrosis with an increase and/or a decrease in a patient's plasma of cardiac troponin(cT n) with at least one cT n measurement greater than the 99 th percentile of the upper normal reference limit during:(1) symptoms of myocardialischemia;(2) new significant electrocardiogram(ECG) ST-segment/T-wave changes or left bundle branch block;(3) the development of pathological ECG Q waves;(4) new loss of viable myocardium or regional wall motion abnormality identified by an imaging procedure; or(5) identification of intracoronary thrombus by angiography or autopsy.Myocardial infarction,when diagnosed,is now classified into five types.Detection of a rise and a fall of troponin are essential to the diagnosis of acute MI.However,high sensitivity troponin assays can increase the sensitivity but decrease the specificity of MI diagnosis.The ECG remains a cornerstone in the diagnosis of MI and should be frequently repeated,especially if the initial ECG is not diagnostic of MI.There have been significant advances in adjunctive pharmacotherapy,procedural techniques and stent technology in the treatment of patients with MIs.The routine use of antiplatelet agents such as clopidogrel,prasugrel or ticagrelor,in addition to aspirin,reduces patient morbidity and mortality.Percutaneous coronary intervention(PCI) in a timely manner is the primary treatment of patients with acute ST segment elevation MI.Drug eluting coronary stents are safe and beneficial with primary coronary intervention.Treatment with direct thrombin inhibitors during PCI is non-inferior to unfractionated heparin and glycoprotein Ⅱb/Ⅲa receptor antagonists and is associated with a significant reduction in bleeding.The intra-coronary use of a glycoprotein Ⅱb/Ⅲa antagonist can reduce infarct size.Pre- and post-conditioning techniques can provide additional cardioprotection.However,the incidence and mortality due to MI continues to be high despite all these recent advances.The initial ten year experience with autologous human bone marrow mononuclear cells(BMCs) in patients with MI showed modest but significant increases in left ventricular(LV) ejection fraction,decreases in LV endsystolic volume and reductions in MI size.These studies established that the intramyocardial or intracoronary administration of stem cells is safe.However,many of these studies consisted of small numbers of patients who were not randomized to BMCs or placebo.The recent LateT ime,Time,and Swiss Multicenter Trials in patientswith MI did not demonstrate significant improvement in patient LV ejection fraction with BMCs in comparison with placebo.Possible explanations include the early use of PCI in these patients,heterogeneous BMC populations which died prematurely from patients with chronic ischemic disease,red blood cell contamination which decreases BMC renewal,and heparin which decreases BMC migration.In contrast,cardiac stem cells from the right atrial appendage and ventricular septum and apex in the SCIPIO and CADUCEUS Trials appear to reduce patient MI size and increase viable myocardium.Additional clinical studies with cardiac stem cells are in progress. | Koushik Reddy Asma Khaliq Robert J Henning | 2015 | World Journal of Cardiology2015，7，5： | 107 |
| 2 | Ischemia/reperfusion injury and cardioprotective mechanisms:Role of mitochondria and reactive oxygen species显示文摘Reperfusion therapy must be applied as soon as possible to attenuate the ischemic insult of acute myocardial infarction(AMI).However reperfusion is responsible for additional myocardial damage,which likely involves opening of the mitochondrial permeability transition pore(mPTP).In reperfusion injury,mitochondrial damage is a determining factor in causing loss of cardiomyocyte function and viability.Major mechanisms of mitochondrial dysfunction include the long lasting opening of mPTPs and the oxidative stress resulting from formation of reactive oxygen species(ROS).Several signaling cardioprotective pathways are activated by stimuli such as preconditioning and postconditioning,obtained with brief intermittent ischemia or with pharmacological agents.These pathways converge on a common target,the mitochondria,to preserve their function after ischemia/reperfusion.The present review discusses the role of mitochondria in cardioprotection,especially the involvement of adenosine triphosphate-dependent potassium channels,ROS signaling,and the mPTP.Ischemic postconditioning has emerged as a new way to target the mitochondria,and to drastically reduce lethal reperfusion injury.Several clinical studies using ischemic postconditioning during angioplasty now support its protective effects,and an interesting alternative is pharmacological postconditioning.In fact ischemic postconditioning and the mPTP desensitizer,cyclosporine A,have been shown to induce comparable protection in AMI patients. | Maria-Giulia Perrelli Pasquale Pagliaro Claudia Penna | 2011 | World Journal of Cardiology2011，3，6： | 64 |
| 3 | Sevoflurane postconditioning reduces myocardial reperfusion injury in rat isolated hearts via activation of PI3K/Akt signaling and modulation of Bcl-2 family proteins显示文摘Sevoflurane postconditioning reduces myocardial infarct size.The objective of this study was to examine the role of the phosphatidylinositol-3-kinase(PI3K)/Akt pathway in anesthetic postconditioning and to determine whether PI3K/Akt signaling modulates the expression of pro-and antiapoptotic proteins in sevoflurane postconditioning.Isolated and perfused rat hearts were prepared first,and then randomly assigned to the following groups:Sham-operation(Sham),ischemia/reperfusion(Con),sevoflurane postconditioning(SPC),Sham plus 100 nmol/L wortmannin(Sham+Wort),Con+Wort,SPC+Wort,and Con+dimethylsulphoxide(DMSO).Sevoflurane postconditioning was induced by administration of sevoflurane(2.5%,v/v) for 10 min from the onset of reperfusion.Left ventricular developed pressure(LVDP),left ventricular end-diastolic pressure(LVEDP),maximum increase in rate of LVDP(+dP/dt),maximum decrease in rate of LVDP(?dP/dt),heart rate(HR),and coronary flow(CF) were measured at baseline,R30 min(30 min of reperfusion),R60 min,R90 min,and R120 min.Creatine kinase(CK) and lactate dehydrogenase(LDH) were measured after 5 min and 10 min reperfusion.Infarct size was determined by triphenyltetrazolium chloride staining at the end of reperfusion.Total Akt and phosphorylated Akt(phospho-Akt),Bax,Bcl-2,Bad,and phospho-Bad were determined by Western blot analysis.Analysis of variance(ANOVA) and Student-Newman-Keuls' test were used to investigate the significance of differences between groups.The LVDP,±dP/dt,and CF were higher and LVEDP was lower in the SPC group than in the Con group at all points of reperfusion(P<0.05).The SPC group had significantly reduced CK and LDH release and decreased infarct size compared with the Con group [(22.9±8)% vs.(42.4±9.4)%,respectively;P<0.05].The SPC group also had increased the expression of phospho-Akt,Bcl-2,and phospho-Bad,and decreased the expression of Bax.Wortmannin abolished the cardioprotection of sevoflurane postconditioning.Sevoflurane postconditioning may protect the isolated rat heart.Activation of PI3K and modulation of the expression of pro-and antiapoptotic proteins may play an important role in sevoflurane-induced myocardial protection. | Li-na YU Jing YU Feng-jiang ZHANG Mei-juan YANG Ting-ting DING Jun-kuan WANG Wei HE Tao FANG Gang CHEN Min YAN | 2010 | Journal of Zhejiang University-Science B(Biomedicine & Biotechnology)2010，11，9： | 36 |
| 4 | Cardioprotection and pharmacological therapies in acute myocardial infarction: Challenges in the current era显示文摘In patients with an acute ST-segment elevation myocardial infarction, timely myocardial reperfusion using primary percutaneous coronary intervention is the most effective therapy for limiting myocardial infarct size, preserving left-ventricular systolic function and reducing the onset of heart failure. Within minutes after the restoration of blood flow, however, reperfusion itself results in additional damage, also known as myocardial ischemia-reperfusion injury. An improved understanding of the pathophysiological mechanisms underlying reperfusion injury has resulted in the identification ofseveral promising pharmacological(cyclosporin-A, exenatide, glucose-insulin-potassium, atrial natriuretic peptide, adenosine, abciximab, erythropoietin, metoprolol and melatonin) therapeutic strategies for reducing the severity of myocardial reperfusion injury. Many of these agents have shown promise in initial proofof-principle clinical studies. In this article, we review the pathophysiology underlying myocardial reperfusion injury and highlight the potential pharmacological interventions which could be used in the future to prevent reperfusion injury and improve clinical outcomes in patients with coronary heart disease. | Alberto Dominguez-Rodriguez Pedro Abreu-Gonzalez Russel J Reiter | 2014 | World Journal of Cardiology2014，6，3： | 18 |
| 5 | Association between delayed cardioprotection of aged rat myocytes and activation of mitogenactivated protein kinase显示文摘Objective To study the cardioprotective effects of hypoxic preconditioning (HPC) on aged rat ventricular myocytes and the cellular mechanism of protection Methods In the model of hypoxia/reoxygenation (H/R) of isolated ventricular myocytes of aged rat, the effects of HPC on aged rat ventricular myocytes against lethal H/R stimulated ischemia/reperfusion (I/R) injury 24 hours later and the changes of mitogen activated protein kinase (MAPK) system were observed in the present study Results HPC attenuated the lactate dehydrogenase (LDH) release and ATP depletion in myocytes and increased the viability of myocytes It was also found that MAPK and its down stream kinase—S6 kinase were also activated after HPC Conclusion There is delayed cardioprotection in cardiac myocytes of aged rat and the cellular mechanism underlying might involve the activation of MAPK | 刘秀华 王士雯 武旭东 唐朝枢 | 2000 | Chinese Medical Journal2000，，1： | 14 |
| 6 | Cardioprotective mechanism of SGLT2 inhibitor against myocardial infarction is through reduction of autosis显示文摘Sodium-glucose cotransporter 2(SGLT2)inhibitors reduce cardiovascular mortality in patients with diabetes mellitus but the protective mechanism remains elusive.Here we demonstrated that the SGLT2 inhibitor,Empagliflozin(EMPA),suppresses cardiomyocytes autosis(autophagic cell death)to confer cardioprotective effects.Using myocardial infarction(Ml)mouse models with and without diabetes mellitus,EMPA treatment significantly reduced infarct size,and myocardial fibrosis,thereby leading to improved cardiac function and survival.In the context of ischemia and nutritional glucose deprivation where autosis is already highly stimulated,EMPA directly inhibits the activity of the Na^(+)/H^(+)exchanger 1(NHE1)in the cardiomyocytes to regulate excessive autophagy.Knockdown of NHE1 significantly rescued glucose deprivation-induced autosis.In contrast,overexpression of NHE1 aggravated the cardiomyocytes death in response to starvation,which was effectively rescued by EMPA treatment.Furthermore,in vitro and in vivo analysis of NHE1 and Beclin 1 knockout mice validated that EMPA s cardioprotective effects are at least in part through downregulation of autophagic flux.These findings provide new insights for drug development,specifically targeting NHE1 and autosis for ventricular remodeling and heart failure after Ml in both diabetic and non-diabetic patients. | Kai Jiang Yue Xu Dandan Wang Feng Chen Zizhuo Tu Jie Qian Sheng Xu Yixiang Xu John Hwa Jian Li Hongcai Shang Yaozu Xiang | 2022 | Protein & Cell2022，13，5： | 13 |
| 7 | Protective effect of hyperoside on cardiac ischemia reperfusion injury through inhibition of ER stress and activation of Nrf2 signaling显示文摘Objective:To study the protective effect of hyperoside(Hyp) on cardiac ischemia reperfusion injury and its potential mechanism.Methods:Rats were divided into two groups for the evaluation,the Hyp(50 uM Hyp;n=8) and the control group(n=8).Rat hearts were isolated and perfused with Krebs-Henseleit buffer(KHB) for 30 min.After being inhibited with cardioplegic solution,they were stored for 4 h in B21 solution at 4℃.Afterwards,rat hearts were perfused with KHB again for 45 min.In this period.Hyp was added into solutions of cardioplegia for storage and KHB.Parameters of cardiac functions,including heart rate,the systolic pressure of the left ventricle,the end-diastolic pressure of the left ventricle,the developed pressure of the left ventricle,the left-ventricular systolic pressure and the peak rise rate of the pressure of the left ventricle were recorded.The levels of adenosine triphosphate(ATP),the content of malondialdehyde and apoptotic cells were determined to evaluate the protective effect of Hyp on hearts suffered from ischemia reperfusion injury.Moreover,cultured cardiac myocytes were subjected to the process simulating ischemia/reperfusion.What were analyzed included the endoplasmic reticulum(ER) stress hallmarks expressions,such as binding immunoglobulin protein and C/EBP homologous protein,using the western blot and real-time PCR.Besides,the NF-E2-related factor 2(Nrf2) expression was measured to explore the potential mechanism.Results:Compared with the control group,the Hyp group had better cardiac functional parameters and higher ATP levels;pretreatment of Hyp greatly relieved the apoptosis of myocyte,decreased oxidative stress as well as ER stress and activated the signaling pathway of anti-oxidative Nrf2 to a further extent.Conclusions:Hyp plays an important role in preserving cardiac function by improving ATP levels of tissue,easing oxidative injury of myocardium and reducing apoptosis following IRI dramatically,while the ER stress inhibition and the downstream Nrf2 signaling activation may contribute to the effects of protection. | Jia-Yin Hou Ying Liu Liang Liu Xin-Ming Li | 2016 | Asian Pacific Journal of Tropical Medicine2016，9，1： | 13 |
| 8 | Activation of Akt and cardioprotection against reperfusion injury are maximal with only five minutes of sevoflurane postconditioning in isolated rat hearts显示文摘It had been proved that administration of sevoflurane for the first two minutes of reperfusion effectively protects the heart against reperfusion injury in rats in vivo.Our aim was to investigate the duration of effective sevoflurane administration and its underlying mechanism in isolated rat hearts exposed to global ischemia/reperfusion(I/R) injury.Adult male Sprague-Dawley rats were randomly divided into six groups(n=12):a sham-operation group,an I/R group,and four sevoflurane postconditioning groups(S2,S5,S10,and S15).In the S2,S5,S10,and S15 groups,the duration times of sevoflurane administration were 2,5,10,and 15 min after the onset of reperfusion,respectively.The isolated rat hearts were mounted on the Langendorff system,and after a period of equilibrium were subjected to 40 min global ischemia and 120 min reperfusion.Left ventricular(LV) hemodynamic parameters were monitored throughout each experiment and the data at 30 min of equilibrium and 30,60,90,and 120 min of reperfusion were analyzed.Myocardial infarct size at the end of reperfusion(n=7 in each group) and the expression of myocardial phosphorylated Akt(p-Akt) after 15-min reperfusion were determined in a duplicate set of six groups of rat hearts(n=5 in each group).Compared with the I/R group,the S5,S10,and S15 groups had significantly improved left ventricular end-diastolic pressure(LVEDP),left ventricular developed pressure(LVDP),and the maximal rate of rise or fall of the LV pressure(±dP/dtmax),and decreased myocardial infarct size(P<0.05),but not the S2 group.After 15 min of reperfusion,the expression of p-Akt was markedly up-regulated in the S5,S10,and S15 groups compared with that in the I/R group(P<0.05),but not in the S2 group.Sevoflurane postconditioning for 5 min was sufficient to activate Akt and exert maximal cardioprotection against I/R injury in isolated rat hearts. | Yuan-yuan YAO Man-hua ZHU Feng-jiang ZHANG Chuan-yun WEN Lei-lei MA Wen-na WANG Can-can WANG Xian-bao LIU Li-na YU Ling-bo QIAN Jian-an WANG Min YAN | 2013 | Journal of Zhejiang University-Science B(Biomedicine & Biotechnology)2013，14，6： | 8 |
| 9 | Reducing the oxidative stress mediates the cardioprotection of bicyclol against ischemia-reperfusion injury in rats显示文摘Objective:To investigate the beneficial effect of bicyclol on rat hearts subjected to ischemia-reperfusion(IR) injuries and its possible mechanism.Methods:Male Sprague-Dawley rats were intragastrically administered with bicyclol(25,50 or 100 mg/(kg·d)) for 3 d.Myocardial IR was produced by occlusion of the coronary artery for 1 h and reperfusion for 3 h.Left ventricular hemodynamics was continuously monitored.At the end of reperfusion,myocardial infarct was measured by 2,3,5-triphenyltetrazolium chloride(TTC) staining,and serum lactate dehydrogenase(LDH) level and myocardial superoxide dismutase(SOD) activity were determined by spectrophotometry.Isolated ventricular myocytes from adult rats were exposed to 60 min anoxia and 30 min reoxygenation to simulate IR injuries.After reperfusion,cell viability was determined with trypan blue;reactive oxygen species(ROS) and mitochondrial membrane potential of the cardiomyocytes were measured with the fluorescent probe.The mitochondrial permeability transition pore(mPTP) opening induced by Ca2+(200 μmol/L) was measured with the absorbance at 520 nm in the isolated myocardial mitochondria.Results:Low dose of bicyclol(25 mg/(kg·d)) had no significant improving effect on all cardiac parameters,whereas pretreatment with high bicyclol markedly reduced the myocardial infarct and improved the left ventricular contractility in the myocardium exposed to IR(P<0.05).Medium dose of bicyclol(50 mg/(kg·d)) markedly improved the myocardial contractility,left ventricular myocyte viability,and SOD activity,as well decreased infarct size,serum LDH level,ROS production,and mitochondrial membrane potential in rat myocardium exposed to IR.The reduction of ventricular myocyte viability in IR group was inhibited by pretreatment with 50 and 100 mg/(kg·d) bicyclol(P<0.05 vs.IR),but not by 25 mg/(kg·d) bicyclol.The opening of mPTP evoked by Ca2+ was significantly inhibited by medium bicyclol.Conclusions:Bicyclol exerts cardioprotection against IR injury,at least,via reducing oxidative stress and its subsequent mPTP opening. | Jie CUI Zhi LI Ling-bo QIAN Qin GAO Jue WANG Meng XUE Xiao-e LOU Iain C.BRUCE Qiang XIA Hui-ping WANG | 2013 | Journal of Zhejiang University-Science B(Biomedicine & Biotechnology)2013，14，6： | 8 |
| 10 | Late cardioprotection of exercise preconditioning against exhaustive exercise-induced myocardial injury by up-regulatation of connexin 43 expression in rat hearts显示文摘Objective: To investigate the expression of myocardium connexin 43(Cx43) in late exercise preconditioning(LEP) cardioprotection. Methods: Eight-week-old adult male Sprague Dawley rats were randomly assigned into four groups(n=8). Myocardial injury was judged in accordance with serum levels of c Tn and NT-pro BNP as well as hematoxylin basicfuchsin picric acid staining of myocardium. Cx43 m RNA was detected by in situ hybridization and qualified by real-time fluorescence quantitative PCR. Cx43 protein was localized by immunohistochemistry and its expression level was determined by western blotting. Results: The LEP obviously attenuated the myocardial ischemia/hypoxia injury caused by exhaustive exercise. There was no significant difference of Cx43 m RNA level between the four groups. Cx43 protein level was decreased significantly in group EE(P<0.05). However, LEP produced a significant increase in Cx43 protein level(P<0.05), and the decreased Cx43 protein level in exhaustive exercise was significantly up-regulated by LEP(P<0.05). Conclusions: LEP protects rat heart against exhaustive exercise-induced myocardial injury by up-regulating the expression of myocardial Cx43. | Kai Wang Bai-Chao Xu Hai-Yun Duan Hua Zhang Fu-Song Hu | 2015 | Asian Pacific Journal of Tropical Medicine2015，8，8： | 4 |
| 11 | The epigenetic landscape of exercise in cardiac health and disease显示文摘With the rising incidence of cardiovascular diseases,the concomitant mortality and morbidity impose huge burdens on quality of life and societal costs.It is generally accepted that physical inactivity is one of the major risk factors for cardiac disease and that exercise benefits the heart in both physiological and pathologic conditions.However,the molecular mechanisms governing the cardioprotective effects exerted by exercise remain incompletely understood.Most recently,an increasing number of studies indicate the involvement of epigenetic modifications in the promotion of cardiac health and prevention of cardiac disease.Exercise and other lifestyle factors extensively induce epigenetic modifications,including DNA/RNA methylation,histone post-translational modifications,and non-coding RNAs in multiple tissues,which may contribute to their positive effects in human health and diseases.In addition,several studies have shown that maternal or paternal exercise prevents age-associated or high-fat dietinduced metabolic dysfunction in the offspring,reinforcing the importance of epigenetics in mediating the beneficial effects of exercise.It has been shown that exercise can directly modify cardiac epigenetics to promote cardiac health and protect the heart against various pathological processes,or it can modify epigenetics in other tissues,which reduces the risk of cardiac disease and affords cardioprotection through exerkines.An in-depth understanding of the epigenetic landscape of cardioprotective response to exercise will provide new therapeutic targets for cardiac diseases.This review,therefore,aimed to acquaint the cardiac community with the rapidly advancing and evolving field of exercise and epigenetics. | Guiling Wu Xing Zhang Feng Gao | 2021 | Journal of Sport and Health Science2021，10，6： | 3 |
| 12 | Cardio- and hepato-protective potential of methanolic extract of Syzygium cumini(L.) Skeels seeds:A diabetic rat model study显示文摘Objective: To evaluate the effect of methanolic extract of Syzygium cumini(L.) Skeels(S. cumini) seeds on the major organs in an animal model of diabetes through biochemical and histopathological studies.Methods: The methanolic extracts of S. cumini seeds(100 and 200 mg/kg body weight) were administered to alloxan-induced diabetic rats daily, with fasting blood glucose levels being measured by glucometry at one-day interval for a duration of two weeks. Biochemical assays to evaluate changes in the functions of the heart, liver,pancreas and kidney were carried out. Histopathological changes in the diabetic rat organs(pancreas, liver, heart, kidney and spleen) were also observed after the 14 days of treatment with the extracts.Results: Oral administration of methanolic extracts of S. cumini seeds(100 and 200 mg/kg body weight), with gliclazide as a positive control(25 mg/kg), showed beneficial effects including lowering blood glucose levels(P < 0.001), improved heart and liver functions, and hyperlipidemia due to diabetes. At 200 mg/kg, the extracts reversed cardiac and liver damage caused by alloxan.Conclusions: In addition to the anti-hyperglycemic activity of methanolic extracts of S. cumini seeds, the extracts demonstrates potential to minimize cardiac and hepatic complications. | Sumaiya Nahid Kishor Mazumder Zillur Rahman Saiful Islam Md. Humayun Rashid Philip Grey Kerr | 2017 | Asian Pacific Journal of Tropical Biomedicine2017，7，2： | 2 |
| 13 | Effect of Xuebijing injection on myocardium during cardiopulmonary bypass:A prospective,randomized,double blind trial显示文摘BACKGROUND Cardiopulmonary bypass(CPB)is an essential procedure for maintaining the blood supply to vital organs in patients undergoing cardiac surgery.However,perioperative cardiac injury related to CPB remains a severe complication in these patients.Cardiac protection is important for patients undergoing CPB.AIM To evaluate the potential cardioprotective efficacy of the Chinese medicine preparation Xuebijing injection(XBJ)in patients undergoing CPB.METHODS Sixty patients undergoing cardiac surgery with CPB were randomly allocated to the XBJ and control groups(saline).XBJ was administered intravenously three times:12 h prior to surgery,at the beginning of the surgery,and 12 h after the second injection.Cardiac function was evaluated by echocardiography 48 h after surgery.Circulating inflammation-and oxidative-stress-related markers were measured.Clinical outcomes related to intensive care unit(ICU)stay were recorded.RESULTS Compared to control treatment,XBJ was associated with improved PaO2/FiO2 and cardiac systolic function,but reduced troponin I and creatine kinase fraction after surgery(all P<0.05).The circulating concentrations of tumor necrosis factor-α,interleukin(IL)-1βand IL-8 in the XBJ group were significantly lower than those in the control group(all P<0.05),whereas the circulating concentration of IL-10 was significantly higher in the XBJ group(P<0.05).In addition,the lengths of ICU stay and hospitalization after surgery tended to be shorter in the XBJ group than in the control group,although the differences were not significant.CONCLUSION Perioperative administration of XBJ was associated with attenuated cardiac injury during CPB,likely via anti-inflammatory and antioxidative mechanisms. | Zhe-Hao Jin Xiao-Qing Zhao Hai-Bin Sun Jing-Li Zhu Wei Gao | 2022 | World Journal of Clinical Cases2022，10，13： | 1 |
| 14 | Tolterodine reduces veratridine-augmented late/Na, reverse-/Ncx and early afterdepolarizations in isolated rabbit ventricular myocytes显示文摘扩大近来钠电流(我 Na.L )不仅引起细胞内部的 Na +累积,它在经由 Na +/Ca2+的反向的模式的细胞内部的 Ca 2+超载的结果交换电流(颠倒--我 NCX ),而且延长 APD 并且导致早 afterdepolarizations ( EAD ),它能导致心律不齐和心脏的机能障碍。因此,抑制我 Na.L 被认为是为在局部缺血和心失败的治疗学的干预的一个潜在的方法。在这研究,我们调查了 tolterodine (Tol ) 的效果,一个竞争 muscarinic 受体对手,在扩充的正常和 veratridine (Ver ) 上我 Na.L , 颠倒 -- 我 在孤立的兔子的 NCX 和 APD 室的 myocytes,它可能贡献它的 cardioprotective activity.Methods:兔子室的 myocytes 被准备。我 Na.L 和颠倒 -- 我 NCX 在电压被记录夹钳模式,而行动潜力和导致 Ver 的早 afterdepolarizations (EAD ) 在电流被记录,夹钳模式。药经由 superfusion.Results 被使用:Tol (3-120 nmol/L ) concentration-dependently 禁止了正常并且扩充 Ver 我 有 32.08 nmol/L 和 42.47 nmol/L 的 IC 50 价值的 Na.L 分别地。颠茄碱(100 μ mol/L ) 没影响 Tol (30 nmol/L ) 的禁止的效果在上扩充 Ver 我 Na.L 。相反, Tol 的高集中被需要禁止短暂的钠电流(我 有 183.03 μ 的 IC 50 价值的 Na.T ) ; mol/L。另外, Tol (30 nmol/L ) 显著地转移了 inactivation 曲线我 向没有影响它的激活特征的一个更多的动摇的膜潜力的 Na.T 。而且, Tol (30 nmol/L ) 显著地减少了扩充 Ver 的颠倒 -- 我 NCX 。Tol (30 nmol/L ) 在基础条件下面增加了行动潜力持续时间(APD )16% 。Ver (20 μ mol/L ) 更加扩大了 APD 并且在 18/24 房间(75%) 唤起了 EAD。面对 Ver, Tol (30 nmol/L ) 显著地减少了 APD 和消除 EAD (0/24 房间).Conclusion:Tol 禁止正常、扩充 Ver 我 NaL 和减少扩充 Ver 的颠倒 -- 我 NCX 。另外, Tol 颠倒 APD 的延伸并且消除 Ver 导致的 EAD,因此阻止导致 Ver 的心律不齐。 | Chao WANG Lei-lei WANG Chi ZHANG Zhen-zhen CAO An-tao LUO Pei-hua ZHANG Xin-rong FAN Ji-hua MA | 2016 | Acta Pharmacologica Sinica2016，37，11： | 1 |
| 15 | Is the combinational administration of doxorubicin and glutathione a reasonable proposal?显示文摘The combinational administration of antioxidants and chemotherapeutic agents during conventional cancer treatment is among one of the most controversial areas in oncology. Although the data on the combinational usage of doxorubicin (DOX) and glutathione (GSH) agents have been explored for over 20 years, the duration, administration route, and authentic rationality have not yet been fully understood yet. In the current study, we systematically investigated the pharmacokinetics (PK) and pharmacodynamics (PD) with both in vivo and in vitro models to elucidate the infiuence of GSH on the toxicity and efficacy of DOX. We first studied the cardioprotective and hepatoprotective effects of GSH in Balb/c mice, H9c2, and HL7702 cells. We showed that coadministration of exogenous GSH (5, 50, and 500 mg/kg per day, intragastric) significantly attenuated DOX-induced cardiotoxicity and hepatotoxicity by increasing intracellular GSH levels, whereas the elevated GSH concentrations did not affect the exposure of DOX in mouse heart and liver. From PK and PD perspectives, then the infiuences of GSH on the chemotherapeutic efficacy of DOX were investigated in xenografted nude mice and cancer cell models, including MCF-7, HepG2, and Caco-2 cells, which revealed that administration of exogenous GSH dose-dependently attenuated the anticancer efficacy of DOX in vivo and in vitro, although the elevated GSH levels neither infiuenced the concentration of DOX in tumors in vivo, nor the uptake of DOX in MCF-7 tumor cells in vitro. Based on the results we suggest that the combined administration of GSH and DOX should be contraindicated during chemotherapy unless DOX has caused serious hepatotoxicity and cardiotoxicity. | Bo-yu Shen Chong Chen Yang-fan Xu Jia-jia Shen Hui-min Guo Hao-feng Li Xi-nuo Li Dian Kang Yu-hao Shao Zhang-pei Zhu Xiao-xi Yin Lin Xie Guang-ji Wang Yan Liang | 2019 | Acta Pharmacologica Sinica2019，40，5： | 0 |
| 16 | Effects of dexmedetomidine on cardioprotection and other postoperative complications in elderly patients after cardiac and non-cardiac surgerie显示文摘BACKGROUND After cardiac and non-cardiac surgeries,elderly patients have a high probability of developing cardiac complications and postoperative delirium.Although several clinical trials have investigated whether perioperative intravenous dexmedetomidine can protect the heart and reduce postoperative complications such as delirium in elderly patients,the obtained results have been inconsistent.We conducted a meta-analysis to investigate the effects of dexmedetomidine on cardioprotection and other postoperative complications in elderly patients undergoing cardiac or non-cardiac surgery.AIM To investigate the effects of dexmedetomidine on cardiac complications and delirium in elderly patients undergoing cardiac or non-cardiac surgery.METHODS The PubMed,Cochrane Library,web of science,and other sources were comprehensively searched for all randomized controlled trials published before May 2021 that investigated the efficacy of dexmedetomidine in the prevention of cardiac and postoperative delirium(POD).RESULTS In total,18 studies involving 1025 patients were included in the meta-analysis.Intravenous dexmedetomidine significantly reduced cardiac troponin I(cTnI)and the inflammatory factor tumor necrosis factor-α(TNF-α)was comparable to the control group.Dexmedetomidine also reduced the POD and mortality rates.However,patients in the dexmedetomidine group were more likely to have a decreased heart rate(within the normal range)and hypotension during dexmedetomidine administration than those in the control group.There was no difference in the occurrence of myocardial infarction,bradycardia,or stroke between the two groups.Dexmedetomidine significantly shortened the time to extubate;however,it did not shorten the length of stay in the intensive care unit.CONCLUSION The administration of dexmedetomidine during cardiac and non-cardiac surgeries can provide myocardial protection by inhibiting inflammation and cTnI,which may be beneficial for the rapid recovery of patients.Meanwhile,the administration of dexmedetomidine reduced the incidence of POD and decreased mortality(in-hospital). | Yang-Liang Yang Bao-Ji Hu Jing Yi Meng-Zhi Pan Peng-Cheng Xie Hong-Wei Duan | 2022 | World Journal of Meta-Analysis2022，10，1： | 0 |
| 17 | Impact of conditioning hyperglycemic on myocardial infarction rats:Cardiac cell survival factors显示文摘While clinical data have suggested that the diabetic heart is more susceptible to ischemic heart disease(IHD),animal data have so far pointed to a lower probability of IHD. Thus,the aim of this present review is to look at these conflicting results and discuss the protective mechanisms that conditioned hyperglycemia may confer to the heart against ischemic injury. Several mechanisms have been proposed to explain the cardioprotective action of high glucose exposure,namely,upregulation of anti-apoptotic factor Bcl-2,inactivation of pro-apoptotic factor bad,and activation of pro-survival factors such as protein kinase B(Akt),vascular endothelial growth factor(VEGF),hypoxia inducible factor-1α and protein kinase C-ε. Indeed,cytosolic increase in Ca2+ concentration,the mitochondrial permeability transition pore,plays a key role in the genesis of ischemic injury. Previous studies have shown that the diabetic heart decreased Na+/Ca2+ and Na+/H+ exchanger activity and as such it accumulates less Ca2+ in cardiomyocyte,thus preventing cardiac injury and the associated heart dysfunctions. In addition,the expression of VEGFin diabetic animals leads to increased capillary density before myocardial infarction. Despite poor prognostic in the long-term,all these results suggest that diabetes mellitus and consequently hyperglycemia may indeed play a cardioprotective role against myocardial infarction in the short term. | Christiane Malfitano Alcione Lescano de Souza Junior Maria Cláudia Irigoyen | 2014 | World Journal of Cardiology2014，6，6： | 0 |
| 18 | Beyond cardiomyocytes:Cellular diversity in the heart's response to exercise显示文摘Cardiomyocytes comprise~70%to 85%of the total volume of the adult mammalian heart but only about 25%to 35%of its total number of cells.Advances in single cell and single nuclei RNA sequencing have greatly facilitated investigation into and increased appreciation of the potential functions of non-cardiomyocytes in the heart.While much of this work has focused on the relationship between non-cardiomyocytes,disease,and the heart's response to pathological stress,it will also be important to understand the roles that these cells play in the healthy heart,cardiac homeostasis,and the response to physiological stress such as exercise.The present review summarizes recent research highlighting dynamic changes in non-cardiomyocytes in response to the physiological stress of exercise.Of particular interest are changes in fibrotic pathways,the cardiac vasculature,and immune or inflammatory cells.In many instances,limited data are available about how specific lineages change in response to exercise or whether the changes observed are functionally important,underscoring the need for further research. | Lena E.Trager Margaret Lyons Alexandra Kuznetsov Cedric Sheffield Kangsan Roh Rebecca Freeman James Rhee J.Sawalla Guseh Haobo Li Anthony Rosenzweig | 2023 | Journal of Sport and Health Science2023，12，4： | 0 |
| 19 | Effects of Chios mastic gum on cardiometabolic risk factors显示文摘Chios mastic gum(CMG),the resin produced by the trunk of Pistachia lentiscus var Chia,has been used for culinary and medicinal purposes since antiquity.Despite the fact that Pistacia species are widely distributed throughout the Mediterranean basin and in the circum-Mediterranean regions,CMG is a distinctive resin of the mastic trees grown exclusively in the southern part of the island of Chios.CMG has been used for centuries as a spice,a cosmetic,but its most important usage has been as a strong phytotherapeutic therapy,primarily for the management of gastrointestinal diseases.Recently,there are studies demonstrating that CMG has hypolipidemic,cardioprotective and antidiabetic properties.Therefore,the aim of the present review is to summarize the existing literature data regarding the potential beneficial effects of CMG on cardiometabolic risk factors. | Athanasia K Papazafiropoulou | 2022 | World Journal of Diabetes2022，13，11： | 0 |
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