新生儿窒息合并心肌损害血清心肌酶变化(附12例分析)

目的探讨心肌酶水平对窒息新生儿心肌损害的诊断价值。方法将12例窒息新生儿为实验组,另外收集10例同期正常新生儿作为对照组。两组新生儿经股静脉穿刺采血2 ml,分离血清,在24 h内测定心肌酶活性,同时做心电图检查,统计学处理采用t检验。结果两组血清心肌酶测定结果比较显示两组血清心肌酶均值间的差别有显著性意义。窒息组均出现心电图改变。结论血清心肌酶活性测定及心电图检测可作为新生儿窒息后心肌损害的早期监测和诊断的指标,为早期治疗提供依据。

再灌注性心肌死亡

由于缺乏得力的观察手段,长期未能获得致命性再灌注损伤的直接证据。众多药理学干预实验结果充满分歧,新近运用辣根过氧化物酶示踪技术,初步肯定了致命性再灌注损伤的存在。致损因素的持续存在,有力地支持再灌注损伤的持久性。

舒芬太尼后处理对缺血再灌注大鼠肌钙蛋白Ⅰ的影响

目的评价舒芬太尼后处理对缺血再灌注大鼠肌钙蛋白Ⅰ的影响,从而探讨其保护作用。方法健康雄性SD大鼠72只随机分为6组:假手术组(Sham组),缺血再灌注组(I/R组),缺血后处理组(Post组),舒芬太尼后处理组(LS组,MS组,HS组)。于缺血前即刻(T0,基础值)、缺血30 min(T1)、再灌注30 min(T2)、60 min(T3)、90 min(T4)和120 min(T5)时记录心率(HR)和平均动脉压(MAP);再灌注120 min末,随机取6只按照ELISA法测定心肌肌钙蛋白Ⅰ(cTnI)并计算心肌梗死面积(IS/AAR),另外6只进行光镜及电镜细胞形态学观察。结果 HR在各组各个时点比较差异无统计学意义(P>0.05),与Sham组比较,I/R组在T3、T4和T5时MAP均降低(P<0.05),而LS组在T3和T4时均降低(P<0.05);与I/R组相比,Post组、MS组和HS组血清中的cTnI、心肌梗死面积及心肌细胞损伤程度显著降低(P<0.05)。结论舒芬太尼后处理能够减轻在体大鼠心肌缺血再灌注损伤血清中cTnI,从而产生保护作用。

Protective Effects of Zingiberis and Acniti Praeparatae Decoction on Myocardial IschemiaReperfusion Injury in Rats

This study aimed to investigate the protective effects of zin-giberis and acniti praeparatae decoction on oxidative stress injury induced by my-ocardial ischemia reperfusion in rats. [Method] Myocardial ischemia-reperfusion was performed by ligation of the left anterior descending coronary artery for 30 min, fol-lowed by reperfusion for 60 min. The effects of zingiberis and acniti praeparatae decoction on ECG ST segment, myocardial infarction percentage, malondialdehyde （MDA） content in the serum, superoxide dismutase （SOD） activity and other indica-tors were observed. [Result] Zingiberis and acniti praeparatae decoction could effec-tively inhibit ECG ST segment elevation caused by myocardial ischemia-reperfusion injuries, reduce the percentage of myocardial infarction, decline the content of MDA in the serum, and increase the activity of SOD. [Conclusion] Zingiberis and acniti praeparatae decoction exhibits protective effects on oxidative injuries caused by my-ocardial ischemia-reperfusion injuries in rats, which may be involved in reducing the formation of myocardial free radicals and enhancing antioxidant capacity of my-ocardium.

动脉导管未闭结扎术中扩血管药物的选择与对比研究

目的 对比不同血管扩张药物在动脉导管未闭（PDA）结扎术中的应用效果。方法 选取我院收治的20例患儿作为研究对象,随机分为A组、B组,每组各10例,所有患儿均行左外侧开胸手术,分离动脉导管,常规降压后,丝线结扎。A组给予硝酸甘油,B组采用法舒地尔,用法与A组基本相同,3-5 ng/（kg·min）持续泵入,调节泵入速度。结果 治疗后24 h,与治疗前对比,A组、B组cTnT、CK-MB均高于术前,且A组患者cTnT、CK-MB均高于B组,差异有统计学意义（P〈0.05）,手术成功率100%。结论 PDA结扎术中应用法舒地尔有助于减轻心肌损伤。

MYOCARDIAL LESIONS AFTER LONG-TERM ADMINISTRATION OF METHAMPHETAMINE IN RATS

Objective To demonstrate the myocardial lesion associated with long-term administration of methamphetamine in rats. Methods The experimental models of intoxication of methamphetamine were established in Sprague-Dawley rats. Methamphetamine hydrochloride （3 mg·kg^-1·d^-1） was subcutaneously injected to rats in methamphetarnine-treated group （n = 16）, and normal saline at the same dose was injected to rats in control group （n = 16）. After 1 week and 8 weeks of injection, 8 rats in each group were sacrificed and their hearts were examined with light microscopy and electron microscopy, respectively. Results After 1 week of methamphetamine exposure, loci of contraction band and cellular degeneration were present in subendocardial myocardium. Cellular degeneration, myocytolysis, and contraction band necrosis became prominent and extensive in methamphetamine-treated rats after 8 weeks. Hypertrophy, intracellular vacuolization, and fibrosis were also observed. The ultrastructural feature showed marked swelling and degeneration of mitochondria, enlargement of sarcoplasmic reticulum, and dissolution of myofilaments. No obvious cardiac myocyte lesions were observed in rats of control group. Conclusion Methamphetamine abuse daily for a long time may result in an increased risk of cardiovascular lesions similar to cardiomyopatby.

C-reactive protein aggravates myocardial ischemia/reperfusion injury through activation of extracellular-signal-regulated kinase 1/2

Background Ischemia/reperfusion injury （IRI） is an inflammatory response that occurs when tissue is reperfused following a prolonged period of ischemia. Several studies have indicated that C-reactive protein （CRP） might play an important role in inducing IRI. However, the effects of CRP on myocardial IRI and the underlying mechanisms have not been fully elucidated. This study aimed to investigate the association between CRP and myocardial IRI and the underlying mechanisms. Methods We simulated ischemia/reperfusion using oxygen-glucose deprivation/ reoxygenation （OGD/R） in neonatal Sprague-Dawley rat cardiomyocytes; reperfusion injury was induced by three hours of hypoxia with glucose and serum deprivation followed by one hour of reperfusion. Cell viability was tested with MTS assays, and cardiomyocyte damage was evaluated by lactate dehydrogenase （LDH） leakage. Mitochondrial membrane potential was measured using tetramethylrhodamine ethyl ester （TMRE） and mitochondrial permeability transition pore （mPTP） opening was measured using calcein/AM; both TMRE and caocein/AM were visualized with laser scanning confocal microscopy. In addition, we studied the signaling pathways underlying CRP-mediated ischemia/reperfusion injury via Western blot analysis. Results Compared with the simple OGD/R group, after intervention with 10 pg/mL CRP, cell viability decreased markedly （82.36 % ± 6.18% vs. 64.84% ± 4.06%, P = 0.0007）, and the LDH leakage significantly increased （145.3 U/L ± 16.06 U/L vs. 208.2 U/L ± 19.23 U/L, P = 0.0122）. CRP also activated mPTP opening and reduced mitochondrial membrane potential during myocardial ischemia/reperfusion. Pretreatment with 1 pM atorvastatin （Ator） before CRP intervention protected cardiomyocytes from IRI. Mitochondrial KATP channel opener diazoxide and mPTP inhibitor cyclosporin A also offset the effects of CRP in this process. The level of phosphorylated extracellular-signal-regulated kinase （ERK） 1/2 was significantly higher after pre-treatment with CRP compared with the OGD/R group （170.4% ± 3.00% v.v. 93.53% ± 1.94%, P 〈 0.0001）. Western blot analysis revealed that Akt expression was markedly activated （184.2% ± 6.96% vs. 122.7% ± 5.30%, P = 0.0003） and ERK 1/2 phosphorylation significantly reduced after co-treatment with Ator and CRP compared with the level after CRP pretreatment alone. Conclusions Our results suggested that CRP directly aggravates myocardial IRI in myocardial cells and that this effect is primarily mediated by inhibiting mitochondrial ATP- sensitive potassium （mitoKATp） channels and promoting mPTP opening. Ator counteracts these effects and can reduce CRP-induced IRI. One of the mechanisms of CRP-induced IRI may be related to the sustained activation of the ERK signaling pathway.

QUANTITATIVE ASSESSMENT OF MYOCARDIAL PERFUSION DEFECTS WITH REAL-TIME THREE-DIMENSIONAL MYOCARDIAL CONTRAST ECHOCARDIOGRAPHY

Objective To evaluate the feasibility and accuracy of measurement of myocardial perfusion defects with intravenous contrast-enhanced real-time three-dimensional echocardiography (CE-RT3DE). Methods RT3DE was performed in 21 open-chest mongrel dogs undergoing acute ligation of the left anterior descending artery (LAD, n=14) or distal branch of the left circumflex artery (LCX, n=7). A perfluorocarbon microbubble contrast agent was injected intravenously to assess the resulting myocardial perfusion defects with Philips Sonos-7500 ultrasound system. Evans blue dye was injected into the occluded coronary artery for subsequent anatomic identification of underperfused myocardium. In vitro anatomic measurement of myocardial mass after removal of the animal’s heart was regarded as the control. Blinded off-line calculation of left ventricular mass and perfusion defect mass from RT3DE images were performed using an interactive aided-manual tracing technique.Results Total left ventricular (LV) myocardial mass ranged from 38.9 to 78.5 (mean±SD: 60.0±10.1) g. The mass of perfusion defect ranged from 0 to 21.4 (mean±SD: 12.0±5.0) g or 0 to 27% of total LV mass (mean±SD: 19%±6%). The RT3DE estimation of total LV mass (mean±SD: 59.8±9.9 g) strongly correlated with the anatomic measurement (r=0.98; y=2.01+0.96x). The CE-RT3DE calculation of the mass of underperfused myocardium (mean±SD: 12.3±5.3 g) also strongly correlated with the anatomic measurement (r=0.96; y=-0.10+1.04x) and when expressed as percentage of total LV mass (r=0.95; y=-0.20+1.04x). Conclusions RT3DE with myocardial contrast opacification could accurately estimate underperfused myocardial mass in dogs of acute coronary occlusion and would play an important role in quantitative assessment of myocardial perfusion defects in patients with coronary artery disease.

Cholecystokinin octapeptide improves cardiac function by activating Cholecystokinin octapeptide receptor in endotoxic shock rats

AIM: To explore the effect of sulfated cholecystokinin octapeptide (sCCK-8) on cardiac functions and its receptor mechanism in endotoxic shock (ES) rats. METHODS: The changes of the mean arterial pressure (MAP), heart rate (HR), the left ventricular pressure (LVP) and the maximal/minimum rate of LVP (±LVdp/dt max) were measured by using physiological record instrument in eight groups of rats. The expression of cholecystokinin-A receptor (CCK-AR) and cholecystokinin-B receptor (CCK-BR) mRNA of myocardium in ES rats was examined by reverse transcription polymerase chain reaction (RT-PCR). RESULTS: (1) Low doses of sCCK-8 (0.4 μg/kg) caused tachycardia (441±27, normal control 391±22 s/min) and slight increase in MAP, LVP and ±LVdp/dtmax (16.96±1.79, 18.21±1.69 and +768.85±31.28/-565.04±27.71 kPa, respectively, all P<0.01), while medium doses (4.0 μg/kg) and high doses of sCCK-8 (40 μg/kg) elicited bradycardia and marked increase in MAP, LVP and ±LVdp/dtmax (17.29±1.63, 19.46±2.57 and +831.46±22.57/-606.08 ±31.32; 17.46±1.08, 19.83±2.91 and +914.52±35.95/ -639.15±30.23 kPa, respectively, all P<0.01). Proglumide (1.0 mg/kg), a nonselective antagonist of CCK-receptor (CCK-R), significantly inhibited the pressor effects of sCCK-8 (15.96±1.38, 17.36±0.66 and +748.18±19.29/-512.12±14.39 kPa, respectively, all P<0.01), whilst reversing the bradycardiac responses. (2) High doses of LPS (8 mg/kg) elicited marked decrease in MAP, LVP and ±LVdp/dtmax. (7.16±0.59, 7.6±0.68 and +298.01±25.52/ -166.96±19.25 kPa, respectively, all P<0.01). Pretreatment with sCCK-8 (40 μg/kg) could reverse the decline of cardiac functions (10.71±0.45, 11.7±1.26 and +446.04±67.18/ -347.90±36.98 kPa, respectively, all P<0.01), while proglumide could cause further decline of cardiac function in ES rats (4.71±0.67, 5.58±1.25 and +226.48±15.84/ -142.83±20.23 kPa, respectively, all P<0.01). (3) CCK-A/BR mRNAs were expressed in myocardium of control rats. Gene expression of CCK-AR and CCK-BR significantly increased in myocardium of ES rats. The increase of CCK-AR mRNA induced by LPS began at 0.5 h, peaked at 2 h, kept a high level at 6 h and declined at 12 h, respectively. Similar to CCK-AR mRNA, the expression of CCK-BR mRNA peaked at 2 h and kept a high level at 6 h, but it did not change at the first 0.5 h and was stable at a high level at 12 h. CONCLUSION: The above results indicate that endogenous and exogenous sCCK-8 may significantly improve cardiac function and intractable hypotension of ES rats, which was likely related to high expression of CCK-A/BR in myocardium induced by LPS.

Mechanism of volatile oil from Chuanxiong(Chuanxiong Rhizoma)-Suhexiang(Styrax)-Bingpian(Borneolum)in treating angina pectoris based on network pharmacology and its protective effects on myocardial damage in rats

Objective To explore the pharmacodynamic material basis and mechanism of action of volatile oil from Chuanxiong(Chuanxiong Rhizoma)-Suhexiang(Styrax)-Bingpian(Borneolum)(hereinafter referred to as C-S-B volatile oil)in treating angina pectoris based on network pharmacology and to detect its protective effects against rat myocardial damage.Methods Gas chromatography-mass spectrometry(GC-MS)was used to determine the constituents of volatile oils from Chuanxiong(Chuanxiong Rhizoma),Suhexiang(Styrax),and Bingpian(Borneolum),and the targets of the three main constituents were found predicted and screened using the PharmMapper server,and Gene Cards and Coo LGe N databases.The STRING database and Cytoscape software were used to draw the protein-protein interaction(PPI)network,RStudio software was used to analyze Gene Ontology(GO)and Kyoto Encyclopedia of Genome and Genome(KEGG)pathways,and Cytoscape software was used to construct the component-target-pathwaydisease network.The rat model of myocardial injury was established by intraperitoneal injection of a large dose of isoprenaline hydrochloride.After continuous intervention with C-S-B volatile oil for 14 d,the ejection fraction(EF)and short axis shortening rate(FS)of the left ventricle were detected.The indices of myocardial damage were detected after hematoxylin-eosin(HE)staining.Results Fifteen volatile oil components from the C-S-B formula were identified.There are 470 targets of these volatile oil components and 401 angina-related genes.There are 28 core targets,including CHRM4,ADRA1 A,FGFR1,CHRM2,CYP2 A6,CHRM5,CHRM1,CHRM3,HDAC2,and MPO,etc..The results of the KEGG analysis indicated that the C-S-B formula probably interferes with the following pathways:neuroactive ligand-receptor interactions,calcium signaling,cytochrome P450 metabolism of heteropoietin,among others.The results of animal experiments showed that the C-S-B formula essential oil could significantly improve the following myocardial indices in rats with myocardial injury:EF,FS,left ventricular end-systolic diameter(LVIDs),left ventricular end-diastolic diameter(LVIDd),and stroke volume(SV),and all the differences were statistically significant(P<0.01).Conclusion The mechanism of action of volatile oil components in the C-S-B formula in treating angina pectoris was analyzed using multi-component,multi-target and multi-pathway systems,which has laid a foundation for further revealing its mechanism of action.Animal experiments have shown that the volatile oil of the C-S-B formula can improve EF,FS,and other indices of myocardial damage in a rat model,thus relieving myocardial damage caused by heart hyperactivity,improving cardiac function,and protecting against myocardial damage.

Mediated protective effect of electroacupuncture pretreatment by miR-214 on myocardial ischemia/reperfusion injury

Background Electroacupuncture pretreatment plays a protective role in myocardial ischemia/reperfusion （I/R） injury and microRNAs （miRNAs） could act on various facets of cardiac function. However, the role of miRNAs in the cardioprotection by electroacupuncture pre-treatment on myocardial I/R injury remains unknown. The purpose of the study was to examine whether miR-214 was involved in cardio-protection by electroacupuncture. Methods Using rat myocardial I/R model, we examined the role of electroacupuncture pretreatment in myocardial I/R injury and analyzed the changes in the expression of miR-214. In addition, I/R was simulated in vitro by performing oxy-gen-glucose deprivation （OGD） on H9c2 cell cultures, and the effect of electroacupuncture pretreatment on I/R injury as well as expressional level of miR-214 were examined in vitro. Furthermore, the miR-214 mimic was transfected into OGD-treated H9c2 cells, we analyzed the cell apoptosis, lactate dehydrogenase （LDH） and creatine kinase （CK） activities, intracellular free Ca2＋concentration （[Ca2＋]i） as well as the relative protein levels of sodium/calcium exchanger 1（NCX1）, BCL2-like 11 （BIM）, calmodulin-dependent protein kinase IIδ（CaMKIIδ） and Cyclophilin D （CypD）. Results The in vivo results revealed that compared with the I/R group, the electroacupuncture pretreatment group showed significant decreased myocardial infarct size, as well as the increased indices of the cardiac function, including heart rate, mean arterial pressure, left ventricular systolic pressure and maximal rate for left ventricular pressure rising and declining （±dp/dt max）. In addition, electroacupuncture pretreatment could inhibit the elevation of LDH and CK activities induced by I/R injury. The quantitative PCR （qPCR） results demonstrated electroacupuncture pretreatment could provide cardioprotection against myocardial I/R injury in rats with miR-214 up-regulation. In the meanwhile, in vitro, electroacupuncture pretreatment protected H9c2 cells from OGD-induced injury. Trans-fection of miR-214 mimic showed protective effects on OGD-induced injury to H9c2 cells by reducing apoptosis, decreasing LDH and CK activities, rescuing the OGD-induced Ca2＋and down-regulating elevated protein levels of NCX1, BIM, CaMKIIδand CypD. Conclusions Our findings firstly demonstrated that electroacupuncture pretreatment promotes the expression of miR-214 in myocardial I/R injury and miR-214 contributes to the protective effect of electroacupuncture on myocardial I/R injury.

Effect of shenfu injection on gastrointestinal microcirculation in rabbits after myocardial ischemia-reperfusion injury

AIM： To investigate the effect of shenfu injection on gastrointestinal microcirculation after myocardial ischemic-reperfusion （IR） injury in rabbits and probe into the mechanism. METHODS： Forty healthy flap-eared white rabbits were randomly divided into 4 groups： IR injury control group （group Ⅰ ）, shenfu injection 5 mL/kg per h group （group Ⅱ）, shenfu injection 10 mL/kg per h group （group Ⅲ） and shenfu injection 20 mL/kg per h group （group Ⅳ）. The four groups were treated with Lactated Ringer＇s solution, shenfu injection 5, 10, and 20 mL/ kg per h were infused intravenously 30 min before experiment respectively. The values of hemodynamics [mean arterial pressure （MAP）, heart rate （HR）, gastric intramucosal partial pressure of carbon dioxide （PCO2）, blood gas analysis and pH] were measured and compared with those before myocardial ischemia, 60 min after myocardial ischemia and 60, 90, and 180 rain after reperfusion. RESULTS： The MAP, HR and gastric intramucosal pH were （70.50 ± 4.50） kPa, （165 ± 14） beats per rain, 7.032 ± 0.024 in group Ⅰ 60 min after myocardial ischemia, which were significantly decreased compared with those before myocardial ischemia （88.50 ± 9.75 kPa, 217 ± 18 beats per rain, 7.112 ± 0.035, P 〈 0.05）. The MAP, HR and gastric intramucosal pH were significantly decreased in group Ⅰ 60, 90, and 180 min after reperfusion （61.50 ± 5.25 kPa, 133 ± 31 beats per rain, 6.997 ± 0.025） compared with those before reperfusion respectively （P 〈 0.05）, whereas the values were insignificantly different in groups Ⅱ, Ⅲ or Ⅳ after reperfusion, compared with those before reperfusion, and there were no significant differences between groups Ⅱ, Ⅲ, and Ⅳ after reperfusion. CONCLUSION： Pre-infusion of shenfu injection has a protective effect on gastrointestinal microcirculation after myocardial IR injury in rabbits, in a dose independent manner.

The role and modulation of autophagy in experimental models of myocardial ischemia-reperfusion injury

A physiological sequence called autophagy qualitatively determines cellular viability by removing protein aggregates and damaged cyto-plasmic constituents, and contributes significantly to the degree of myocardial ischemia-reperfusion （I/R） injury. This tightly orchestrated cata-bolic cellular‘housekeeping’ process provides cells with a new source of energy to adapt to stressful conditions. This process was first described as a pro-survival mechanism, but increasing evidence suggests that it can also lead to the demise of the cell. Autophagy has been implicated in the pathogenesis of multiple cardiac conditions including myocardial I/R injury. However, a debate persists as to whether autophagy acts as a protec-tive mechanism or contributes to the injurious effects of I/R injury in the heart. This controversy may stem from several factors including the va-riability in the experimental models and species, and the methodology used to assess autophagy. This review provides updated knowledge on the modulation and role of autophagy in isolated cardiac cells subjected to I/R, and the growing interest towards manipulating autophagy to increase the survival of cardiac myocytes under conditions of stress-most notably being I/R injury. Perturbation of this evolutionarily conserved intracellular cleansing autophagy mechanism, by targeted modulation through, among others, mammalian target of rapamycin （mTOR） inhibitors, adenosine monophosphate-activated protein kinase （AMPK） modulators, calcium lowering agents, resveratrol, longevinex, sirtuin activators, the proapoptotic gene Bnip3, IP3 and lysosome inhibitors, may confer resistance to heart cells against I/R induced cell death. Thus, therapeutic ma-nipulation of autophagy in the challenged myocardium may benefit post-infarction cardiac healing and remodeling.

MicroRNA-15a/b are up-regulated in response to myocardial ischemia/reperfusion injury

Objective Several studies have indicated that miR-15a,miR-15b and miR-16 may be the important regulators of apoptosis.Since attenuate apoptosis could protect myocardium and reduce infarction size,the present study was aimed to find out whether these miRNAs participate in regulating myocardial ischemia reperfusion （I/R） injury.Methods Apoptosis in mice hearts subjected to I/R was detected by TUNEL assay in vivo,while flow cytometry analysis followed by Annexin V/PI double stain in vitro was used to detect apoptosis in cultured cardiomyocytes which were subjected to hypoxia/reoxygenation （H/R）.Taqman real-time quantitative PCR was used to confirm whether miR-15a/15b/16 were involved in the regulation of cardiac I/R and H/R.Results Compared to those of the controls,I/R or H/R induced apoptosis of cardiomyocytes was significantly iucreased both in vivo （24.4％ ± 9.4％ vs.2.2％ ± 1.9％,P ＜ 0.01,n =5） and in vitro （14.12％ ±0.92％ vs.2.22％ ± 0.08％）.The expression of miR-15a and miR-15b,but not miR-16,was increased in the mice I/R model,and the results were consistent in the H/R model.Conclusions Our data indicate miR-15 and miR-15b are up-regulated in response to cardiac I/R injury,therefore,down-regulation of miR- 15a/b may be a promising strategy to reduce myocardial apoptosis induced by cardiac I/R injury.

PROTECTIVE EFFECTS OF MELATONIN ON CULTURED RAT CARDIOMYOCYTES DAMAGED BY H_2O_2

Objective.To investigate the protective effects of melatonin(MT )on cardiomyocytes against the ox-idative injury induced by H 2 O 2 .Methods.Ventricular myocytes were isolated from neonatal rats and cultured for3～5days.Cells were divided into4groups:control group,H 2 O 2 (100μmol/L H 2 O 2 )group,MT group(100μmol/L MT )and MT preconditioning group(100μmol/L MT+100μmol/L H 2 O 2 ).The fluorescent probe,DCFH?DA,was used to detect intracellular levels of reactive oxygen species(ROS)and another fluorescent probe,Fluo-3?AM,was used to detect[Ca 2+ ] i by using a laser scanning confocal microscopy(LSCM).The malondi-aldehyde(MDA)content in cardiomyocytes was determined by measuring thiobarbituric acid?reactive sub-stances to monitor lipid peroxidation.The activity of cytoplasmic enzyme lactate dehydrogenase(LDH)that was released into the culture media was assayed to indicate alternation in the integrity of the cellular membrane.Trypan blue exclusion was used to detect the cell viability.Results.Compared with the control group,intracellular ROS,[Ca 2+ ] i ,MDA content ,LDH leakage and cell death were significantly elevated when cells were treated by100μmol/L H 2 O 2 for60minutes(P<0.01).However,those changes were significantly attenuated in MT preconditioning group.Conclusion.MT has very good antioxidant effect and can protect the cardiomyocytes against H 2 O 2 -in-duced injury.

EFFECT OF COXSACKIEVIRUS B3 ON ION CHANNEL CURRENTS IN RAT VENTRICULAR MYOCYTES

To investigate the effects of coxsackievirus B 3(CVB 3) on ion channel currents in rat ventricular myocytes. Methods.Rat hearts were isolated with collagenase to acquire single ventricular myocytes, L type voltage dependent calcium channel(VDCC)current (I Ca ),Na + current (I Na ), outward potassium current (I out ), inwardly rectifying potassium current(I KI ) were recorded using whole cell patch clamp techniques. ResultsCVB 3 infection increased I Ca and I out , while decreased I KI ; but it had no obvious effect on I Na . Conclusion.The effects of CVB 3 on I Ca 、 I out 、 I KI may be one of the mechanisms of myocytes damage and the occurrence of abnormal electroactivities induced by CVB 3 infection.

急性脑血管病血清脑型利钠肽改变61例临床分析

目的:通过检测血清脑型利钠肽(BNP)水平,探讨血清BNP对急性脑血管病风险分析和预后判断的意义。方法:对61例急性脑血管病患者进行血清脑型利钠肽(BNP)水平改变分析,随访3个月。结果:健康对照组BNP63.84±20.13pmol/ml,与无意识障碍组(147.12±29.14pmol/ml)和意识障碍组(426.68±79.82pmol/ml)相比,均显著增高(P<0.01),且无意识障碍组和意识障碍组相比有统计学显著差异(P<0.01)。

IMPLANTATION OF AUTOLOGOUS BONE MARROW MONONUCLEAR CELLS INTO ISCHEMIC MYOCARDIUM ENHANCES CORONARY CAPILLARIES AND SYSTOLIC FUNCTION IN MINISWINE

Objective To investigate the therapeutic effectiveness of intracoronary implantation of autologous bone marrow mononuclear cells (BM-MNC) in miniswine model of reperfused myocardial infarction. Methods Sixteen miniswine myocardial ischemic reperfusion injury models made by ligation of the distal one third segment of left anterior descending artery for 90 minutes were randomized into 2 groups. In BM-MNC group (n = 9), (3.54±0.90)×108 BM-MNC were intracoronary injected, and in the control group (n = 7), phosphate buffered saline was injected by the same way. Echocardiographic and hemodynamic results, vessel density, and myocardial infarction size were evaluated and compared before and 4 weeks after cell transplantation. Results In BM-MNC group, there were no differences between before and 4 weeks after transplantation in aspects of left ventricular ejection fraction (LVEF), interventricular septal thickness, left ventricular lateral and anterior septal wall thickness, cardiac output, or +dp/dtmax. In control group, LVEF, interventricular septal thickness, left ventricular lateral and anterior septal wall thickness, cardiac output, and +dp/dtmax decreased significantly 4 weeks after transplantation (P < 0.05). Left ventricular end-diastolic pressure and –dp/dtmax did not change significantly before and after cell transplantation in both groups. Capillary density in BM-MNC group was greater than that in control group [(13.39 ± 6.96)/high power field vs. (3.50 ± 1.90)/high power field, P < 0.05]. Infarction area assessed by tetrazolium red staining and the infarction percentage decreased in BM-MNC group compared with those in control group (P < 0.05). Conclusions Transplantation of BM-MNC into myocardium with ischemic reperfusion injury increases capillary density and decreases infarction area. It has significantly beneficial effect on cardiac systolic function rather than on diastolic function.

The therapeutic effect of Jiawei Danshen Decoction on myocardial ischemia-reperfusion injury by inhibiting H_(2)S-mediated autophagy signaling pathway

Objective To investigate the protective effects of Jiawei Danshen Decoction(加味丹参饮,JWDSD)on myocardial ischemia-reperfusion injury(MIRI)via the regulation of serum Hydrogen sulfide(H2S)and cardiac Beclin1,light Chain 3 A/B(LC3 A/B),p62,and autophagy protein5(ATG5).Methods Seventy specific pathogen free(SPF)Sprague-Dawley(SD)rats were randomly assigned to seven groups(n=10 in each group),including normal control,sham operation,MIRI model(model),ischemic preconditioning,Na HS,JWDSD,and JWDSD+CSE inhibitor(JWDSD+PPG)groups,and orally administered the indicated drugs for 14 d.Two hours after the last administration,the left anterior decreased branch of the coronary artery of each rat in model,Na HS,JWDSD,and JWDSD+PPG groups was ligated for 30 min and subsequently reperfused for 90 min to establish the MIRI model,and the rats in the sham operation group were only exposed to the thorax after surgery without coronary ligation.Blood samples were collected to detect H2S levels using an enzyme-linked immunosorbent assay(ELISA).Heart tissues were harvested for histopathological and immunohistochemical examination and quantitative reverse transcription polymerase chain reaction analysis of Beclin1 and ATG5 m RNA expression and Western blot analysis of Beclin1,LC3 A/B,and p62 protein expression.Results(1)The serum H2S content in model group rats was significantly reduced(P<0.01),JWDSD significantly increased the serum H2S content of model group rats(P<0.01),and the CSE inhibitor(PPG)significantly reduced H2S levels in the JWDSD group rats(P<0.01).(2)Compared with the normal control group,the myocardial tissue necrosis and cell destruction occurred in the MIRI model group,and JWDSD could alleviate the myocardial tissue necrosis of model rats,but the ameliorative effect of JWDSD could be reversed by PPG.(3)Beclin1,LC3 A/B,and p62 expression levels in the heart tissues of the model group were significantly increased(P<0.001),whereas decreased by JWDSD(P<0.05,P<0.01,and P<0.001,respectively),and the inhibitory effects of JWDSD on Beclin1,LC3 A/B,and p62 expression were partially reversed by PPG(P<0.01,P<0.05,and P<0.01,respectively).(4)The expression levels of autophagy-related genes Beclin1 and ATG5 were significantly increased in the model group(P<0.001).JWDSD clearly downregulated the expression levels of Beclin1 and ATG5(P<0.05 and P<0.001,respectively),which were reversed by PPG(P<0.001).Conclusion Our experimental data show that JWDSD can exhibit an anti-MIRI role by increasing endogenous H2S generation,and downregulating the expression of Beclin1,LC3 A/B,p62 and ATG5,which are related to inhibiting autophagy signaling.