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.
We present three patients who underwent repeat aortic valve replacement for prosthetic valve dysfunction caused by tissue ingrowth in the late postoperative period. These patients (three women aged 48-51 years, mean 49.3 +/- 1.53 years) underwent operations for restriction of prosthetic valve leaflet movement by pannus in the left ventricular outflow tract. The interval from the previous operation ranged from 8.0 to 9.6 years (mean 9.6 +/- 2.0 years). The symptoms of the patients were New York Heart Association functional class I, II, and IV in one patient each. Diagnosis was made by cinefluoroscopy in two patients and aortography in one patient. The operative procedures consisted of aortic valve replacement ( n = 1) and aortic valve replacement with mitral valve replacement ( n = 2). Pannus was found at the left ventricular aspect of the prosthetic valve in all patients. In two patients, the pannus directly restricted movement of the leaflet and also severely narrowed the inflow orifice of the prosthetic valve. In the other patient, the pannus had grown at a distance of 7 mm from the valve and narrowed the left ventricular outflow tract circularly. The postoperative course was uneventful and all three patients were discharged in a good condition. One patient died of pneumonia 8 months after surgery and the other two patients have remained well and have been followed up for one and a half years. In conclusion, there may be a discrepancy between the clinical symptoms and the grade of subvalvular stenosis caused by pannus. Therefore, it is essential for satisfactory operative results that early diagnosis be made by various means.
Nine cases of mycotic thoracic aortic aneurysm were treated surgically between July 1995 and March 2003. The aneurysms were located in the ascending aorta in 1 patient, the descending thoracic aorta in 5, and the thoracoabdominal aorta in 3. Preoperatively, 3 patients were in shock due to rupture of the aneurysm. All patients underwent aneurysmectomy and in-situ graft placement. In 5 patients, the graft was covered with a pedicled omental flap to prevent postoperative graft infection. There were 2 hospital deaths: one patient died of multi-organ failure, and the other died from intrathoracic bleeding. After discharge, one patient died from intrathoracic bleeding 3 months after surgery. These 3 patients had not received omental wrapping. Postoperative graft infection did not occur in the 6 surviving patients during a mean follow-up period of 4.0 +/- 3.1 years. It was concluded that covering the prosthetic graft with a pedicled omental flap may help prevent postoperative graft infection and improve the surgical results.
Prevention of cerebral injury is an important consideration during repair of aortic arch aneurysm, and the major goal of cerebral protection techniques. We describe our surgical strategy for treatment of extended thoracic aortic aneurysms. Between January 2001 and June 2008, 17 men and 6 women, with a mean age of 67.9 +/- 8.3 years, underwent total replacement of the arch and descending aorta. Six (26.1%) patients required emergency surgery. A median sternotomy with a left anterolateral thoracotomy provided a good visual field, and bilateral axillary arteries were preferentially used for systemic as well as selective cerebral perfusion. Two (8.7%) patients died in hospital. Prolonged mechanical ventilation was required for 7.3 +/- 8.4 days after surgery in 17 patients who all recovered uneventfully. Permanent neurological dysfunction developed in 1 (4.3%) patient who died of sepsis 2 years after the operation. Our results suggest that total arch replacement through a median sternotomy plus a left anterolateral thoracotomy is helpful for extended replacement of the thoracic aorta as well as distal reoperation for dissecting type A aortic aneurysm. Perfusion via bilateral axillary arteries may improve cerebral protection.
The efficacy of transcranial myogenic motor-evoked potential (tc-MEP) monitoring during thoracic aortic surgery has been the subject of some reports, because tc-MEP monitoring can rapidly reflect changes in spinal cord blood flow during thoracic aortic cross-clamping. In this article, we present a case in which delayed loss of tc-MEP signals was observed after cross-clamping of the descending thoracic aorta. We must be aware that tc-MEPs recorded from the lower extremities can fail to provide rapid detection of spinal cord ischemia in the upper thoracic level after cross-clamping of the descending thoracic aorta.
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