Loading...
  • arrest
  • 1997. Out-of-hospital cardiac arrest in the 1990s: a population-based study in the Maastricht area on incidence, characteristics and survival. (springer.com)
  • left anteri
  • Methods and Results- To determine the role of Abcc6 in cardioprotection, we induced ischemic injury in mice in vivo by occluding the left anterior descending artery (30 minutes) followed by reperfusion (48 hours). (ahajournals.org)
  • Methods and results: Using an ischaemia/reperfusion mouse model (left anterior descending artery ligated for 1 h) we achieved remarkable protection of the reperfused tissue with Targ-CD39 compared with Non-targ-CD39 (mutated, non-binding version of Targ-CD39) and PBS control. (monash.edu)
  • Through this enrichment at activated platelets, the required systemic dose is below the dose impairing haemostasis.Methods and results: Using an ischaemia/reperfusion mouse model (left anterior descending artery ligated for 1 h) we achieved remarkable protection of the reperfused tissue with Targ-CD39 compared with Non-targ-CD39 (mutated, non-binding version of Targ-CD39) and PBS control. (monash.edu)
  • global ischemia
  • Methods: Ex vivo rat heart perfusions were performed with Krebs-Henseleit buffer containing 33 mM glucose vs. controls (11 mM glucose) for 60 min stabilization, followed by 20 min global ischemia and 60 min reperfusion ± 5 µM lactacystin and 10 µM MG-132, respectively. (sun.ac.za)
  • significantly
  • When these myocytes were pretreated with urocortin, the ischemia-induced increase in lysophosphatidylcholine concentration was significantly lowered. (ox.ac.uk)
  • inhibition
  • We found that chondroitin sulfate proteoglycans (CSPGs) were present in the infarct after I-R, but not after chronic ischemia, and that CSPGs caused inhibition of sympathetic axon outgrowth in vitro . (jneurosci.org)
  • Conclusion- These data identify Abcc6 as a novel modulator of cardiac myocyte survival after I/R. This cardioprotective mechanism may involve inhibition of the BMP signaling pathway, which modulates apoptosis. (ahajournals.org)
  • Results: The proteasome inhibitor doses and treatment duration here employed resulted in partial UPS inhibition during the reperfusion phase. (sun.ac.za)
  • Furthermore, UPS inhibition leads to a reduction in ventricular tachyarrhythmias [ 17 ] and preserved cardiac function following myocardial ischemia under baseline glucose conditions. (biomedcentral.com)
  • 18 ]. also reported that inhibition of the PI3K/Akt signaling pathway could abolish the effects of B-type natriuretic peptide on myocardial ischemia-reperfusion (I-R) injury. (biomedcentral.com)
  • apoptosis
  • Previous studies had showed that Apelin 13 could protect against apoptosis induced by ischemic/reperfusion (I/R). However, the mechanisms whereby Apelin 13 protected brain I/R remained to be elucidated. (springer.com)
  • ligation
  • Twenty four and 168 hours after IT exposure, cardiac ischemia was induced by left anterior descending coronary artery ligation for 20 minutes followed by 2 hours of reperfusion. (ecu.edu)
  • Metabolic parameters, echocardiography, heart rate variability and then cardiac I/R protocol involving 30-min coronary artery ligation, followed by 120-min reperfusion, were performed. (bioscientifica.com)
  • instillation
  • Exposure to AgNP may result in a sensitization of the immune system in response to a secondary insult (e.g., cardiac I/R) which are largely correlated with capping agents and particle size and may drive expansion of I/R injury at 24 and 168 hours following IT instillation of AgNP. (ecu.edu)
  • Superoxide
  • The proteasome inhibitors also enhanced cardiac superoxide dismutase protein levels (SOD1, SOD2), attenuated pro-inflammatory effects and caused an upregulation of autophagic markers. (sun.ac.za)
  • surgery
  • Intraoperative ECG was monitored throughout cardiac I/R surgery for heart rate (HR), PR interval, and QT interval. (ecu.edu)
  • therapeutic
  • Background: A highly efficient approach to select microRNA (miRNA) targets is a key to develop a miRNA-based therapeutic approach to cardiac ischemia-reperfusion (I/R). To reverse the change induced by disease, I/R in this case, is the traditional strategy to develop therapeutic drugs. (innopsys.com)
  • Conclusion: Mimicking miRNA changes caused by cardioprotective agents, combined with functional screening, enables investigators to efficiently identify novel miRNAs with therapeutic potential in cardiac I/R. (innopsys.com)
  • redox
  • We hypothesize that Cygb modulates cardiac remodeling following IR injury by effecting redox sensitive signaling pathyways (p53, NF-κB, etc). (ahajournals.org)
  • 1997
  • 1997. Out-of-hospital cardiac arrest in the 1990s: a population-based study in the Maastricht area on incidence, characteristics and survival. (springer.com)
  • inhibitor
  • Moreover, co-incubation of cardiac myocytes with urocortin, or the specific phospholipase A2 inhibitor bromoenol lactone, reduces the cytotoxicity produced by lysophosphatidylcholine or ischemia/reperfusion. (ox.ac.uk)
  • cytokines
  • We hypothesized pulmonary exposure to Ag core AgNP induces a measureable increase in circulating cytokines, expansion of cardiac ischemia-reperfusion (I/R) injury and is associated with depressed coronary constrictor and relaxation responses. (rti.org)