Active clinical trials for "Reperfusion Injury"

Rationale: Ischaemic preconditioning (IP) refers to the reduction of ischemia-reperfusion injury induced by a brief preceding period of ischemia. Also the arterial endothelium can be protected by IP. Several studies performed in animals and humans have demonstrated that the protective effects of IP are attenuated with aging. However, no previous study directly examined the underlying mechanisms of this observation. Possibly, the reduced protective effect of IP with aging relates to a direct effect on the endothelium, consequently leading to an attenuated ability of IP to prevent endothelial dysfunction after ischaemia reperfusion injury. Several previous studies failed to demonstrate the ability of pharmacological stimuli to mimic the beneficial effects of IP in aged vessels. Restoration of the age-related reduction in effectiveness of IP may be possible through exercise training. In aged animals, physical training restores the efficacy of ischemic preconditioning. Indirect evidence indicates that physical activity, independent of other cardiovascular risk factors, protects against a occurrence as well as the severity of a myocardial infarction in humans. Although this suggests that physical activity may beneficially influence the age-related reduction in IP, no previous study provided direct evidence for this hypothesis. Objective: To examine the impact of age and physical fitness on the ability of ischaemic preconditioning to protect endothelial damage in response to ischaemia reperfusion injury in healthy humans. A secondary objective is to explore the role of Toll-like receptor (TLR) signalling in the induction of IP in young and old subjects.

Tea consumption may impact upon the decrease in endothelial function after IR-injury. However, no previous study directly examined the potential of tea to impact upon the change in endothelial function after IR-injury. The investigators hypothesize that tea consumption counteracts endothelial damage in response to ischaemia reperfusion injury in healthy humans.

The overall aim of this study is to examine the role of mitochondrial respiration in human diabetic tissue before and after ischemia. Furthermore we will examine the ability of ischemic preconditioning (IPC) to preserve the mitochondrial function and hemodynamic performance of both non-diabetic and diabetic fibers after ischemia. To increase our understanding on the metabolic changes during ischemia in both non-diabetic and diabetic tissue we will use Dimethyl Malonate and examine the impact of this blockade on post-ischemic mitochondrial respiration.

This study aims to understand the impact of time-of-the day on human myocardial tolerance to ischemia-reperfusion by exploring atrial myocardium biopsied during cardiac surgery. Patients scheduled for non-urgent cardiac surgery (coronary artery by-pas graft and/or aortic valve replacement) will be assigned to a morning or an afternoon cardiac surgery based on randomization. Myocardial biopsies will be explored in ex vivo conditions mimicking ischemia-reperfusion.

Severe ischemic changes of the liver remnant after hepatectomy could expedite tumor recurrence on the residual liver. Our study aimed at assessing the effect of warm ischemic/reperfusion (I/R) injuries on surgery-to-local recurrence interval and patient overall survival, during major hepatectomies under inflow and outflow vascular control.

The purpose of this study is to determine whether Remote Ischemic Perconditioning is effective on Acute kidney injury in adult valve replacement.

The study will analyze the incidence, clinical outcomes and predictors of myocardial injury in a large patient population with COVID-19 treated in Mount Sinai Hospital (MSH) system. In addition, the study team will explore the association between high-sensitivity troponin I (TnI) levels and clinical characteristics, biomarkers, cardiac tests data and treatment approaches to uncover the potential mechanisms responsible for COVID-19 induced myocardial injury.

Because of cellular changes in response to ischemia and a following period of reperfusion, damages to organs and different tissues occur. There are several ongoing studies to enlighten the pathophysiological processes underlying these damages inflicted by ischemia/reperfusion. Gases (CO2) with low water content are used in pneumoperitoneum, which is a procedure to inflate the abdominal cavity with an appropriate gas for laparoscopic operations. In the current literature, it was shown that due to a restricted blood flow during the gas insufflation, ischemia develops and with the reperfusion of the organ in deflation period, oxidative stress and inflammation increases, leading to ischemia/reperfusion-related organ and tissue damages. In the proposed study, biomarkers for ischemia/reperfusion-inflicted damage will be evaluated in a biochemical and histopathological perspective in biopsy samples of ovaries from a young patient group in which hysterectomy and bilateral salpingo-oophorectomy will be performed, laparoscopically.

Ischemia/reperfusion injury following aortic cross-clamping for vascular surgery leads to systemic hemodynamic and microcirculatory perturbances. The use of different anesthetic regimens may have an impact on tissue perfusion. The aim of this study was to explore changes in microvascular perfusion in patients undergoing elective open abdominal aortic aneurysm repair under balanced or total intravenous anesthesia. Prospective observational study on 40 patients scheduled for elective open infrarenal abdominal aortic aneurysm repair, who received balanced (desflurane + remifentanil, n=20) or total intravenous anesthesia (TIVA, propofol + remifentanil using target-controlled infusion, n=20) according to the clinician's decision. A goal-directed hemodynamic management was applied in all patients. Hemodynamics and arterial/venous blood gases were compared before anesthesia induction (baseline) and at end-surgery. Changes in sublingual microvascular flow and density were assessed with incident dark field illumination imaging. Near infrared spectroscopy was applied on the thenar eminence with a vascular occlusion test (VOT) to assess variations in the peripheral muscle tissue oxygenation and microcirculatory reactivity.

Background: The cardiomyocytes apoptosis induced by ischemia-reperfusion(I/R) is one of the most important factors in the myocardial I/R injury(MIRI) undergoing cardiac valve replacement with cardiopulmonary bypass(CVRCPB),and Ischemic postconditioning (I-postC) can inhibit apoptosis of myocardial cells. Consequently, this study investigated the key genes and apoptosis signaling pathways of myocardium in patients undergoing CVRCPB. Methods: A total of 36 New York Heart Association class II or III patients with rheumatic heart disease (RHD) of both sexes, aged 21-59 years, who were scheduled for first cardiac valve replacement with CPB in the investigators' hospital from February 2014 to May 2015, were randomly divided into the following three groups (n=12 each): negative control group (NEG group); I/R group (POS group); and I-postC group (Treat group). In the Treat group, the procedure involved 5 min before opening the ascending aorta, aortic unclamping for 30 s, and cross-clamping for 30 s for three cycles, after which the ascending aorta was completely opened. The NEG and Treat groups were not treated. Thirty-six patients were assessed for arrhythmia and recovery of myocardial contractile function after reperfusion by electrocardiograms and degree of dependence on vasoactive drugs. The myocardial tissues of the right atrial appendage were obtained at 3 min before CPB was established in the NEG group, and at 45 min after opening the aorta in the POS and Treat groups. In all three groups, the myocardial tissues of the right atrial appendage were obtained and preserved at -80°C for further experiments. The right atrial appendage of three patients randomly selected in each group was fixed with RNA later (Qiagen, Hilden, Germany) in a centrifuge tube overnight at 4°C, and then preserved at -20°C for RNA extraction. Human 12×135K Gene Array profiling of mRNA expressions was undertaken in human cardiac muscle cells. Differentially expressed mRNAs verified by quantitative real-time RT-PCR were subjected to pathway analysis. The mRNA expressions of AIF, APAF1, CYCS, Bax, caspase-3, caspase-9, caspase-6, caspase-7, BCL2, BAG1, and PI3K were assessed by real-time RT-PCR and western blot analysis. The levels of myocardial apoptosis induced by I/R were investigated by TUNEL assays. The changes in MIRI induced by myocardial apoptosis were investigated by pathologic examination of the myocardium.