Autophagy is a lysosome-dependent degradative pathway which is characterized by cytoplasmic vacuolization. However, it is not just a simple degradative pathway. Research shows that autophagy is related to many diseases, such as neurodegenerative disease, malignant tumor, ageing, pathogenic microorganism infection, myocardial ischemia/reperfusion injury and so on. Autophagy exactly exists in myocardial ischemia/reperfusion injury, and it becomes a new research hotspot. This review will focus on the occurrence and development of autophagy and its role, signal transduction and research status in myocardial ischemia/reperfusion injury.

OBJECTIVE: To evaluate the effect of ?3 Adrenoceptor (?3-AR) antagonist SR59230A(SR) on cardiac function and expression of ?3-AR in rats with heart failure. METHODS: A total of 85 male Wistar rats were enrolled: 8 were as-signed to control group, and 77 were established into heart failure model and then 20 rats that modelled successly assigned ran-domly to placebo group or SR group, with placebo group intraperitoneally injected with normal saline and SR group with SR. The echocardiogram, hemodynamics, and expression of ?3-AR in rats after 7-week treatment were followed. RESULTS: In SR group compared with placebo group, shortening fraction, ejection fraction, left ventricular end systolic pressure, dp/dtmax and dp/dtmin were significantly higher (P

Objective To study the feasibility of using fractional flow reserve (FFR) to guide whether to perform coronary revascularization of non-culprit moderate stenosis in patients with unstable angina and estimate their clinical prognosis. Methods This study enrolled unstable angina patients with multivessel disease. First successful stenting of the culprit artery, then the other non-culprit moderate coronary stenosis were randomized into PCI guided by angiography or guided by FFR measurements. Death from any cause, nonfatal myocardial infarction, unplanned hospitalization leading to urgent revascularization and clinical manifestations with angina were followed during the first year. Results 71 patients were included, among them 35 patiens were randomly assigned to angiography-guided PCI and 36 patients to FFR-guided PCI. In FFR-guided PCI group, FFR was successfully measured in all of non-culprit moderate coronary stenosis. In 23 stenosis, the FFR was greater than 0.80, and stents were not placed in these stenosis. In 13 stenosis with FFR<0.8, stent were inplant and FFR was raised≥0.95 after stenting. The percentage of patients who had a primary end-point event was higher in the angiography-guided PCI group than the FFR-guided PCI group (P<0.05). Neither the rate of mortelity from any cause nor the rate of non-fatal myocardial infarction had significant difference between the 2 groups. Related to the target vessels rates of nonfatal myocardial infarction (5.6%vs. 28.6%) and target lesion revascularization (5.6%vs. 31.4%) were statistically different (P<0.01 and P<0.05, respectively). Conclusions In patients with unstable angina, it is safe to use FFR values to guide decisions on the revascularization of angiographically moderate non-culprit stenosis. Routine measurement of FFR in addition to angiographic guidance, as compared with PCI guided by angiography alone, results in a significant reduction in major adverse events at 1 year, particularly in urgent revascularization, and clinical manifestations with angina get better.

OBJECTIVETo investigate the effect of chronic treatment of enbrel (EB), a TNF-alpha antagonist, in a well defined congestive heart failure (CHF) rat model and test the hypothesis that chronic treatment of EB in CHF rats may limit the progression of Left ventricular (LV) dysfunction and structure remodeling and decrease cardiac IL-1beta levels.

METHODSWe measured cardiac conformation, contractile performance and cytokines level in 8 age-matched normal adult rats (control group) and 8 rats with isoproterenol (ISO)-induced Heart failure (ISO group) and 8 rats with ISO-induced lesion but received EB treatment (EB group).

RESULTSLV end diastolic diameter and LV end systolic diameter in EB group were significantly less and LV fractional shortening was significantly larger than ISO group (9.2 +/- 0.3 mm vs 9.5 +/- 0.2 mm, 5.8 +/- 0.5 mm vs 6.5 +/- 0.3 mm, 0.37 +/- 0.03 vs 0.31 +/- 0.02, P < 0.05, P < 0.01, P < 0.01 respectively , but there was no significant difference of LV posterior wall thickness at end diastole between the two groups; LV end systolic pressure (P(ES)) dp/dt(max) in EB group were significantly greater than ISO group (104.8 +/- 4.6 mm Hg vs 98.4 +/- 4.9 mm Hg, 8395 +/- 940 mm Hg/s vs 6898 +/- 612 mm Hg, P < 0.05 P < 0.01 respectively), and LV end diastolic pressure (P(ED)) dp/dt(min), time constant of LV relaxation were significantly lower than ISO group (3.8 +/- 0.6 mm Hg vs 7.1 +/- 0.8 mm Hg, -5963 +/- 475 mm Hg/s vs-5030 +/- 316 mm Hg/s,15.4 +/- 0.8 ms vs 21.3 +/- 1.4 ms, P < 0.01, respectively . Although cardiac contractile performance in the EB group was greatly improved, there still was a big gap when compared with the control group. The ratio of LV weight to body weight in the EB group was significantly higher than control group 2.82 +/- 0.07 mg/g vs 2.28 +/- 0.08 mg/g, P < 0.01 but there was no significant difference when compared with the ISO group. There was no significant difference between the serum level of TNF-alpha in EB group and ISO group the it could not be detected in control group. TNF-alpha levels in LV of EB group was significantly higher than control group, 757.6 +/- 46.8 pg/g vs 367.5 +/- 22.7 pg/g, P < 0.01 but there was no significant difference when compared with ISO group. The IL-1beta level in LV of EB group was significantly lower than ISO group 356.2 +/- 28.5 pg/g vs 518.4 +/- 32.5 pg/g, P < 0.05 and it could not be detected in control group. The serum level of IL-1beta could not be detected in any rats.

CONCLUSIONEB administered as soon as possible when ISO induced myocardial necrosis occurs can greatly improve cardiac contraction, and the improvement may be partly due to a decrease in the IL-1beta level in LV, besides the direct blocking effect of EB on TNF-alpha. EB can alleviate cardiac remodeling by its effect on LVEDD.

Animals ; Body Weight ; drug effects ; Echocardiography ; Etanercept ; Heart Failure ; diagnostic imaging ; drug therapy ; physiopathology ; Immunoglobulin G ; therapeutic use ; Interleukin-1 ; analysis ; Isoproterenol ; pharmacology ; Male ; Rats ; Rats, Wistar ; Receptors, Tumor Necrosis Factor ; therapeutic use ; Tumor Necrosis Factor-alpha ; analysis ; antagonists & inhibitors ; Ventricular Dysfunction, Left ; prevention & control

Objective:Autoimmune mechanisms, including cellular and humoral immune, are likely to participate in the pathogenesis of at least a subgroup of idiopathic dilated cardiomyopathy(IDC), in which cellular immune-mediated one plays a more important role. Cytotoxic T lymphocyte associated antigen-4(CTLA-4) is the major negative regulatory factor of cellular immunity. This study was conducted to investigate the association of CTLA-4 gene promoter -318C/T polymorphism, exon 1 A/G polymorphism and 3′ untranslated region microsatellite polymorphism with susceptibility to IDC in Han Chinese.Methods:Polymerase chain reaction-restriction fragment length polymorphisms(PCR-RFLP) techniques were used to analyze the polymorphisms of CTLA-4 promoter -318, exon 1 A/G and 3′ untranslated region in the unrelated Han ethnic population in Heilongjiang Province(including 72 IDC patients and 100 normal controls). Serum sCTLA-4 was tested by ELISA. The relationship of CTLA-4 genotype and alleles frequencies with sCTLA-4 was evaluated by linear regression analysis.Results:Compared with controls, the frequencies of GG genotype(0.604 2 and 0.739 6, P=0.012) and the G allele(0.360 0 and 0.560 0, P=0.008) were significantly increased in patients with IDC. Increased serum sCTLA-4 was found in the IDC group compared with the controls[(1.87?1.06)?g/L vs (0.54?0.19)?g/L, P