This study investigated the protective effects of carvedilol, a potent antioxidant, in a rat model of tourniquet-induced ischaemia-reperfusion injury of the hind limb. Thirty rats were divided equally into three groups: the control group (group 1) was only anaesthetized, without creating an ischaemia-reperfusion injury; group 2 was submitted to ischaemia (4 h), followed by a 2-h reperfusion period; and group 3 was pre-treated with carvedilol (2 mg/kg per day) for 10 days prior to ischaemia-reperfusion. Ischaemia-reperfusion produced a significant decrease in superoxide dismutase and glutathione peroxidase activities in the liver, lungs, muscle and serum compared with control treatment, and pre-treatment with carvedilol prevented these changes. Ischaemia-reperfusion caused a significant increase in malondialdehyde and nitric oxide (NO) levels in liver, lungs, muscle (except NO) and serum compared with control treatment, and carvedilol prevented these changes. In conclusion, it might be inferred that carvedilol could be used safely to prevent oxidative injury during reperfusion following ischaemia in humans.

BackgroundVarious types of markers have been used so far in order to reveal myocardial perfusion defect. However, these markers usually appear in the necrosis phase or in the late stage. Having been the focus of various investigations recently, ischemia-modified albumin (IMA) is helpful in establishing diagnosis in the early stages of ischemia, before necrosis develops.Methods and Results30 patients that underwent only coronary bypass surgery due to ischemic heart disease within a specific period of time have been included in the study. IMA levels were studied in the preoperative, intraoperative, and postoperative periods. The albumin cobalt binding assay was used for IMA determination. Hemodynamic parameters (atrial fibrillation, the need for inotropic support, ventricular arrhythmia) of the patients in the postoperative stage were evaluated. Intraoperative measurement values (mean ± SD) of IMA (0.67677 ± 0.09985) were statistically significantly higher than those in the preoperative (0.81516 ± 0.08894) and postoperative (0.70477 ± 0.07523) measurements. Considering atrial fibrillation and need for inotropics, a parallelism was detected with the levels of IMA.ConclusionsIMA is an early-rising marker of cardiac ischemia and enables providing a direction for the treatment at early phases.

Reperfusion injury is a consequence of inadequate energy supply and acidosis in ischemic tissues and a chain of events triggered by oxygen-derived free radicals released in response to exposure of oxygen. In this study, we aimed to assess the effects of clopidogrel, an antithrombotic agent, on experimental ischemia-reperfusion model in rats. The ischemia was performed by blockade of the circulation of right lower extremity at trochanter major level for 6 hours. Then, the extremity was reperfused for 4 hours. Another group of rats pretreated with clopidogrel (0.2 mg/kg/day) for 10 days prior to ischemia-reperfusion. After the reperfusion period, all rats were anesthetized with ketamine. Blood and tissue samples from the gastrocnemius muscle, liver and lungs were taken for the measurement of malondialdehyde (MDA), glutathione (GSH) levels and superoxide dismutase (SOD) activity. The results revealed that clopidogrel prevented the increase in MDA level and the decrease in GSH level and SOD activity caused by ischemia-reperfusion both in tissue samples and plasma. These findings suggest that clopidogrel is beneficial in prevention of ischemia-reperfusion injury probably via its effects on inflammatory cells, platelets, and endothelial cells.

Surgery is indicated for symptomatic patients with papillary fibroelastomas (PFE) on the aortic valve. The valve is commonly spared during tumor excision. Rarely, aortic valve replacement (AVR) is needed. We present a case requiring AVR for an aortic valve PFE and review the literature to determine the risk factors for failure of aortic valve-sparing techniques in patients with PFE.

Ischemia and reperfusion injury is a pathologic process with serious consequences, arising due to interruption of arterial blood flow. Restored blood flow achieved after the ischemic period causes formation of oxygen radicals by activation of a variety of substances and systems. In this study, we investigated the effect of clopidogrel, an antithrombocyte agent, on tissue nitric oxide (NO) levels in an experimental ischemia reperfusion model. For this purpose, 6 hours of ischemia and 4 hours of subsequent reperfusion were applied to the right lower extremities of the subjects. Clopidogrel therapy was started in one of these groups 10 days before the process (study group). NO levels were measured in all groups in the muscle, lung, and liver tissues, and in plasma. Lung, plasma, and liver NO measurement values had statistically significant differences among the groups. There was no statistically significant difference in the measurements made on the muscle tissue. Clopidogrel, which has previously been reported to be suitable to be used as a preventive agent of ischemia reperfusion damage, has had a reducing effect on the NO levels in tissues in the ischemia reperfusion model created in our present study.

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AEF is a catastrophic complication of TEVAR. Conservative treatment is often associated with fatal results. If possible, these patients should be treated with secondary major surgical procedures.

There are various causes of the formation of arterial pseudoaneurysms, including trauma, surgical procedures, infection and iatrogenic injuries. A popliteal aneurysm was detected in a patient with pain and discomfort in his leg. The patient had a history of knee surgery. The aneurysm was treated surgically. Aneurysms following penetrating arterial injury resulting from surgical intervention requiring the use of surgical devices is one of the possible traumatic causes.