We believe that if visceral ischaemia is severe and extensive in patients with type A aortic dissection, abdominal surgery should proceed before the aorta is surgically approached to avoid further irreversible ischaemic damage caused by circulatory arrest in organs with compromised perfusion.
Background: Oxidative stress due to reactive oxygen species (ROS) is thought to play a considerable role in ischemia/reperfusion (I/R) injury that impairs cardiac function. The present study examined oxidative damage in I/R injury and investigated the correlation between oxidative stress and impaired cardiac function after I/R injury of the isolated rat heart. Methods: Hearts isolated from male Sprague-Dawley rats were mounted on a Langendorff apparatus. Hearts arrested using St. Thomas cardioplegic solution and then they were reperfused. The hearts were divided into three groups depending on the frequency (0-2) of I/R. After I/R, left ventricular developed pressure (LVDP), left ventricular end-diastolic pressure (LVEDP), positive maximum left ventricular developing pressure (max LV dP/dt) and coronary flow (CF) were measured. Creatine kinase (CK) was measured in the coronary effluent and 8-hydroxy-2'deoxyguanosine (8OHdG), a marker of oxidative DNA damage, was measured. Adenosine triphosphate (ATP) was measured from frozen myocardial tissue after experiment. Results: We immunohistochemically demonstrated and quantified levels of 8-OHdG after I/ R injury of the heart. The frequency of I/R injury and cardiac dysfunction significantly and negatively correlated. The ATP products were similar among the three groups. The incidence of ventricular arrhythmias was not by affected oxidative stress. Conclusion: The frequency of I/R injury had more of an effect on 8-OHdG products and on impaired cardiac function with less myocyte damage than ischemic duration within 30 minutes of ischemia.Keywords: oxidative stress, ischemia/reperfusion injury, 8-hydroxy-2'deoxyguanosine (8OHdG), cardiac dysfunction tion might cause negative effects and a worse prognosis, with myocardial dysfunction (stunning) and coronary noreflow phenomenon. 1) Reactive oxygen species (ROS), which can be produced from reperfusion of the ischemic myocardium 2) and Ca 2 + overload in myocytes, contribute to cardiac ischemia/reperfusion (I/R) injury.
3)Reactive oxygen species cause the oxidation of DNAs, membranous phospholipids and proteins, and these are implicated in the pathogenesis of I/R injury, degenerative disease, carcinogenesis and aging. In particular, ROS have the potential to injure cardiac myocytes, endothelial cells and initiate chemical reactions in myocardial I/R injury.
Submucosal hematoma of the esophagus is encountered as a rare complication of endoscopic treatment for esophageal varices, but is seen more often with the increasing frequency of endoscopic applications. Idiopathic submucosal hematoma is a rarer event and in most cases sudden intense vomiting has been postulated as its cause. We report here the case of such a patient whose condition was complicated by a dissecting aneurysm. During conservative treatment, careful follow-up was required to differentiate the submucosal hematoma from an aorto-esophageal fistula.
Spinal cord blood flow is positively correlated with mean systemic blood pressure and spinal cord perfusion pressure under spinal cord ischemia caused by clamping a wide range of segmental arteries. In open and endovascular thoracic and thoracoabdominal surgery, elevating mean systemic blood pressure is a simple and effective means of increasing spinal cord blood flow, and measuring spinal cord perfusion pressure seems to be useful for monitoring perioperative spinal cord blood flow.
A right-sided aortic arch associated with an aberrant subclavian artery is a rare anomaly. Regardless, this condition is clinically relevant because mortality is associated with rupture, morbidity results from compression of mediastinal structures, and the surgery is complex. We describe the successful surgical repair of this vascular anomaly by totally debranching the neck vessels and placing an endovascular stent-graft to exclude the ruptured Kommerell's diverticulum.
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