Direct oral anticoagulant agents attenuate temporary aortic occlusion-induced renal oxidative and inflammatory responses in rats.

Background: This study aims to investigate the effects of different direct oral anticoagulants on experimental renal injury induced by temporary infrarenal aortic occlusion. Methods: A total of 35 male Wistar rats (250 to 350 g) were randomly allocated to any of the five groups: sham, ischemia-reperfusion, rivaroxaban, dabigatran, and apixaban groups. Sham group underwent median laparotomy. Ischemia-reperfusion group was given saline gavage for one week. Animals in the other groups received rivaroxaban (3 mg/kg), dabigatran (15 mg/kg), or apixaban (10 mg/kg) daily once for one week via oral gavage. The infrarenal abdominal aorta was clamped for 60 min, and reperfusion was maintained for 120 min in the ischemia-reperfusion, rivaroxaban, dabigatran, and apixaban groups. At the end of reperfusion, kidneys were harvested for biochemical and histopathological analysis. Results: Renal total antioxidant capacity was reduced, and total oxidant status, interleukin-1 beta, and tumor necrosis factor-alpha were elevated in the ischemia-reperfusion group, compared to the sham group (p<0.005). Histological damage scores were also higher in the ischemia-reperfusion group (p<0.005). Administration of direct oral anticoagulants caused an increase of total antioxidant capacity and reduction of total oxidant status, tumor necrosis factor-alpha, and interleukin-1 beta in the rivaroxaban, dabigatran, and apixaban groups compared to the ischemia-reperfusion group (p<0.005). Histological damage scores were lower in the rivaroxaban and dabigatran groups than the ischemia-reperfusion group scores (p<0.005). Conclusion: Direct oral anticoagulants reduce aortic clamping-induced renal tissue oxidation and inflammation. Rivaroxaban and dabigatran attenuate ischemia-reperfusion-related histological damage in kidneys.

Borate reduces experimental supra-celiac aortic clamping-induced oxidative stress in lung and kidney, but fails to prevent organ damage.

BACKGROUND: This study aims to investigate the effects of 2-aminoethoxydiphenyl borate (2-APB) on aortic clamping-induced lung and kidney tissue oxidation, tissue inflammation, and histological damage in a rat model. METHODS: A total of 28 adult female Wistar albino rats were randomly allocated to four equal groups: Control group, ischemia-reperfusion group, dimethyl sulfoxide group, and 2-APB group. Animals in the control group underwent median laparotomy. In the remaining groups, supra-celiac aorta was clamped for 45 min and, then, reperfusion was constituted for 60 min. The 2-APB (2 mg/kg) was administered before clamping. The remaining groups received saline (ischemia-reperfusion group) or dimethyl sulfoxide (dimethyl sulfoxide group). Kidney and lung tissue samples were harvested at the end of reperfusion. RESULTS: Aortic occlusion caused increased tissue total oxidant status and reduced total antioxidant status and glutathione levels in the ischemia-reperfusion and dimethyl sulfoxide groups. Tissue interleukin-1 beta and tumor necrosis factor-alpha levels, nuclear factor kappa beta activation, and histological damage severity scores were also higher in these groups. The 2-APB treatment eliminated the increase in total oxidant status and the decrease in total antioxidant status and glutathione levels. It also caused a decrease in the interleukin-1 beta levels, although it did not significantly alter the tumor necrosis factor-alpha levels, nuclear factor kappa beta immunoreactivity, and histological damage scores. CONCLUSION: Borate exerted a beneficial antioxidant effect as evidenced by reduced oxidative stress; however, it did not inhibit nuclear factor kappa beta activation and prevent histological damage in supra-celiac aortic clamping-induced kidney and lung injury in rats.

Probiotic Saccharomyces boulardii Alleviates Lung Injury by Reduction of Oxidative Stress and Cytokine Response Induced by Supraceliac Aortic Ischemia-Reperfusion Injury in Rats.

OBJECTIVES: Ischemia-reperfusion injury is an important cause of multiple organ failure in cardiovascular surgery. Our aim is to investigate the effect of the probiotic Saccharomyces boulardii on oxidative stress, inflammatory response, and lung injury in an experimental model of aortic clamping. METHODS: Twenty-one Wistar rats were randomized into three groups (n=7). Control group animals received saline gavage for a week before undergoing median laparotomy. In other groups, supraceliac aorta was clamped for 45 minutes to induce ischemia followed by reperfusion for 60 minutes. In the ischemiareperfusion group, saline gavage was given preoperatively for one week. Ischemia-reperfusion+probiotic group rats received probiotic gavage for seven days before aortic clamping. The levels of oxidative stress markers and pro-inflammatory cytokines were determined in both serum and lung tissue samples. Ileum and lung tissues were harvested for histological examination. RESULTS: Ischemia-reperfusion caused severe oxidative damage and inflammation evident by significant increases in malondialdehyde and cytokine levels (tumor necrosis factor alpha and interleukin-1 beta) and decreased glutathione levels in both serum and lung tissues. There was severe histological tissue damage to the lung and ileum in the ischemia-reperfusion group. Probiotic pretreatment before aortic clamping caused significant suppression of increases in serum and lung tissue malondialdehyde and tumor necrosis factor alpha levels. Histological damage scores in tissue samples decreased in the ischemia-reperfusion+probiotic group (P<0,005). CONCLUSIONS: Oral supplementation of probiotic S. boulardii before supraceliac aortic ischemia-reperfusion in rats alleviates lung injury by reducing oxidative stress, intestinal cellular damage, and modulation of inflammatory processes.

TNF-alpha inhibitor adalimumab attenuates endotoxin induced cardiac damage in rats.

PURPOSE: To investigate the effects of adalimumab pretreatment on the lipopolysaccharide-mediated myocardial injury. METHODS: Twenty-eight Wistar rats were randomized into four groups (n=7). Control (C) group animals were injected once a day with intraperitoneal (i.p) 0.9 % saline for two days. In the Adalimumab (Ada) group, adalimumab was injected at a dose of 10 mg/kg/ day (i.p) for two days. Lipopolysaccharide (Lps) group rats were injected with a dose of 5 mg/kg (i.p) lipopolysaccharide. Lipopolysaccharide + Adalimumab (Lps+Ada) group rats received adalimumab before the administration of lipopolysaccharide. The animals were sacrificed 24 h after the last injection and blood samples were obtained for determination of biochemical cardiac injury markers and circulating levels of TNF-α and interleukin-6 (IL-6). Hearts were harvested for histological examination. RESULTS: Endotoxin exposure resulted in significant increases in serum cardiac injury markers, serum cytokines and histological myocardial injury scores in the Lps group. The levels of circulating cytokines, cardiac injury markers and histological injury scores for myocardial necrosis, perivascular cell infiltration, and inflammation were significantly reduced in Lps+Ada as compared to Lps group (p<0.05). CONCLUSIONS: Adalimumab pretreatment reduces endotoxin-induced myocardial damage in rats. This beneficial effect is thought to be related to the reduction of cytokine release.

TNF-alpha inhibitor adalimumab attenuates endotoxin induced cardiac damage in rats

Abstract Purpose To investigate the effects of adalimumab pretreatment on the lipopolysaccharide-mediated myocardial injury. Methods Twenty-eight Wistar rats were randomized into four groups (n=7). Control (C) group animals were injected once a day with intraperitoneal (i.p) 0.9 % saline for two days. In the Adalimumab (Ada) group, adalimumab was injected at a dose of 10 mg/kg/ day (i.p) for two days. Lipopolysaccharide (Lps) group rats were injected with a dose of 5 mg/kg (i.p) lipopolysaccharide. Lipopolysaccharide + Adalimumab (Lps+Ada) group rats received adalimumab before the administration of lipopolysaccharide. The animals were sacrificed 24 h after the last injection and blood samples were obtained for determination of biochemical cardiac injury markers and circulating levels of TNF-α and interleukin-6 (IL-6). Hearts were harvested for histological examination. Results Endotoxin exposure resulted in significant increases in serum cardiac injury markers, serum cytokines and histological myocardial injury scores in the Lps group. The levels of circulating cytokines, cardiac injury markers and histological injury scores for myocardial necrosis, perivascular cell infiltration, and inflammation were significantly reduced in Lps+Ada as compared to Lps group (p<0.05). Conclusions Adalimumab pretreatment reduces endotoxin-induced myocardial damage in rats. This beneficial effect is thought to be related to the reduction of cytokine release.

The effect of ozone treatment on remote organ myocardial injury in an aortic ischemia-reperfusion model.

BACKGROUND: This study aims to investigate the effect of ozone on myocardial ischemia-reperfusion injury occurring after occlusion - reperfusion of infrarenal abdominal aorta in rats. METHODS: Thirty-two Wistar albino rats (weighing 200-250 g) were randomized into four equal groups. The control (sham) group underwent laparotomy and dissection of the infrarenal abdominal aorta without occlusion. Intraperitoneal ozone was applied for 10 days 1 mg/kg/day in the control+ozone group. Afterwards, control+ozone group underwent laparotomy and dissection of the infrarenal abdominal aorta without occlusion. Aortic ischemia-reperfusion and aortic ischemia-reperfusion+ozone groups underwent dissection of the infrarenal abdominal aorta, followed by achieving ischemia and reperfusion by cross-clamping the infrarenal abdominal aorta for 60 minutes and removing the cross-clamp for 60 minutes, respectively. The tissue levels of malondialdehyde and activity levels of superoxide dismutase, catalase, and myeloperoxidase were measured in the myocardial specimens. The tumor necrosis factor, interleukin-6 and troponin-I levels were measured in the plasma. A histopathological examination of the myocardial specimens was undertaken. RESULTS: Biochemical analysis showed that aortic ischemia-reperfusion significantly increased (p<0.05 vs. control) while ozone significantly decreased (p<0.05 vs. aortic ischemia-reperfusion) the myocardial tissue levels of superoxide dismutase and catalase and level of plasma troponin-I. Histologically, in the aortic ischemia-reperfusion group, myocardial disorganization, myofiber swelling and myofiber eosinophilia in the myocardial tissue samples were significantly increased compared to the control group (p<0.05 vs. control). However, histopathological changes in the aortic ischemia-reperfusion+ozone group decreased compared to the aortic ischemia-reperfusion group. CONCLUSION: The results of this experimental study indicate that ozone attenuates myocardial injury and oxidative stress that develop after infrarenal aortic ischemia-reperfusion through three markers; (i) decreased tissue superoxide dismutase and catalase levels, (ii) d ecreased p lasma t roponin-I l evels, a nd (iii) reduced histopathological changes, albeit not statistically significant.

The effects of ozone on bacterial growth and thiol-disulphide homeostasis in vascular graft infection caused by MRSA in rats.

PURPOSE:: To investigate the microbiological, inflammatory and oxidant effects of adjuvant ozone administration in experimental rat vascular graft infection model which has not been previously investigated. METHODS:: Forty adult Wistar rats were divided into Sham, Control, Vancomycin, Ozone, Vancomycin+Ozone groups. Grafts were inoculated with Methicillin-resistant Staphylococcus aureus (MRSA) strain and implanted subcutaneously. Rats were treated intraperitoneally with ozone and /or intramuscularly with vancomycin for 10 days. Grafts were evaluated by quantitative bacterial cultures. Blood samples were harvested for determination of thiol-disulphide and cytokine profiles. RESULTS:: There was no significant difference in bacterial counts between Control and Ozone Groups. In the Ozone Group median colony count was significantly higher than the Vancomycin and Vancomycin+Ozone Groups. Total thiol and disulphide levels increased and disulphide/native thiol and disulphide/total thiol ratios decreased in Ozone Group significantly. Albumin levels decreased significantly in Vancomycin and Vancomycin+Ozone Groups compared to the Sham Group. IL-1 and TNF-alpha levels significantly increased in infected rats. Decreased levels of VEGF due to infection reversed by ozone therapy in control and vancomycin groups. CONCLUSIONS:: We didn't observe any benefit of the agent on MRSA elimination in our model. Likewise, effects of ozone on thiol-disulphide homeostasis and inflammatory cytokines were contradictory.

The effects of ozone on bacterial growth and thiol-disulphide homeostasis in vascular graft infection caused by MRSA in rats

Abstract: Purpose: To investigate the microbiological, inflammatory and oxidant effects of adjuvant ozone administration in experimental rat vascular graft infection model which has not been previously investigated. Methods: Forty adult Wistar rats were divided into Sham, Control, Vancomycin, Ozone, Vancomycin+Ozone groups. Grafts were inoculated with Methicillin-resistant Staphylococcus aureus (MRSA) strain and implanted subcutaneously. Rats were treated intraperitoneally with ozone and /or intramuscularly with vancomycin for 10 days. Grafts were evaluated by quantitative bacterial cultures. Blood samples were harvested for determination of thiol-disulphide and cytokine profiles. Results: There was no significant difference in bacterial counts between Control and Ozone Groups. In the Ozone Group median colony count was significantly higher than the Vancomycin and Vancomycin+Ozone Groups. Total thiol and disulphide levels increased and disulphide/native thiol and disulphide/total thiol ratios decreased in Ozone Group significantly. Albumin levels decreased significantly in Vancomycin and Vancomycin+Ozone Groups compared to the Sham Group. IL-1 and TNF-alpha levels significantly increased in infected rats. Decreased levels of VEGF due to infection reversed by ozone therapy in control and vancomycin groups. Conclusions: We didn't observe any benefit of the agent on MRSA elimination in our model. Likewise, effects of ozone on thiol-disulphide homeostasis and inflammatory cytokines were contradictory.

The relation between compliance to the Mediterranean diet and the extensiveness of coronary artery disease.

OBJECTIVE: There are various studies showing the cardiovascular benefits of the Mediterranean diet (MD), but, to the best of our knowledge, this is the first study which aimed to investigate the relation between adherence to the MD and severity of coronary artery disease (CAD). METHODS: The study was a single centre, cross-sectional prospective study which included 200 consecutive patients (131 men [65.5%] and 69 women [34.5%], mean age 57±9) who were diagnosed with CAD by coronary angiography between January 2012 and April 2013. A food frequency questionnaire was administered to the patients. Compliance to the MD was evaluated by the MD score (MDS), which collects prominent diet characteristics under 10 main titles. Each patient's angiographic data was examined by a cardiologist, and Gensini scores (GS) were then calculated to evaluate the extensiveness of coronary atherosclerosis. RESULTS: Forty-four percent of patients were in the third category of body mass index (BMI) (≥30 kg/m2) and 17.5% were in the first category (BMI<25 kg/m2). Education levels were markedly low, with 78% of the patients having fewer than six years in education. Most patients had low physical activity levels (55.5%). Frequency of metabolic syndrome was prominent (79%). The median (25-75 percentiles) of GS was found to be 21.25 (7-44.75) and the MD score was 4 (3-5). A negative correlation was found between compliance to the MD and GS (r=-0.380, p<0.001). CONCLUSION: This study found that in patients with CAD, compliance with the traditional MD is related to decreased severity of coronary atherosclerosis.

Ozone preconditioning attenuates contrast-induced nephropathy in rats.

BACKGROUND: Contrast-induced nephropathy (CIN) is an important complication of vascular interventions. Ozone therapy can induce tolerance to ischemic insults, a phenomenon known as ozone oxidative preconditioning (OOP). The aim of this study was to investigate the effects of OOP on CIN. MATERIALS AND METHODS: Thirty-two Wistar rats were randomized into four groups (n = 8). The control group had intravenous saline injection. The contrast media (CM) group had intravenous meglumine/sodium diatrizoate injection to form CIN. The ozone (O3) group received intraperitoneal ozone for 5 d before the induction of CIN. The oxygen (O2) group was given an equal amount of oxygen for 5 d before the induction of CIN. The animals were sacrificed 48 h after the administration of contrast agent or saline. Kidneys were harvested, and blood samples were obtained. Renal function tests, serum and renal tissue malondialdehyde (MDA), and nitric oxide (NO) levels and renal oxidant system parameters were determined. Histologic examination was performed for renal injury. RESULTS: Serum blood urea nitrogen (BUN), creatinine, and serum and renal MDA were increased after contrast exposure. Renal NO was decreased, and there was prominent tubular necrosis in the CM group. Serum BUN, creatinine, serum and renal MDA, and grade of tubular necrosis were decreased in the O3 group as compared with those in the CM group. The levels of serum and renal NO and renal total antioxidant system in O3 group were higher than the levels in the CM group. CONCLUSIONS: OOP attenuates experimental CIN. This effect is suggested to be mediated by reinforcement of renal antioxidant defenses and maintenance of renal NO levels.

Influence of preoperative coronary collateral circulation on in-hospital mortality in patients undergoing coronary artery bypass graft surgery with intra-aortic balloon pump support.

BACKGROUND: Outcomes in patients requiring coronary artery bypass graft (CABG) surgery have been improved with devices such as the intra-aortic balloon pump (IABP). Good coronary collateral circulation (CCC) has been shown to reduce mortality in patients with coronary artery disease (CAD). We aimed to investigate whether poor preoperative CCC grade is a predictor of in-hospital mortality in CABG surgery requiring IABP support. METHODS: Fifty-five consecutive patients who were undergoing isolated first time on-pump CABG surgery with IABP support were enrolled into this study and CCC of those patients was evaluated. RESULTS: Twenty-seven patients had poor CCC and 28 patients had good CCC. In-hospital mortality rate in poor CCC group was significantly higher than good CCC group (14 (50%) vs. 4 (13%), P = 0.013). Preoperative hemoglobin level (OR: 0.752; 95% CI, 0.571-0.991, P = 0.043), chronic obstructive pulmonary disease (OR: 6.731; 95% CI, 1.159-39.085, P = 0.034) and poor CCC grade (OR: 5.750; 95% CI, 1.575±20.986, P = 0.008) were associated with post-CABG in-hospital mortality. Poor CCC grade (OR: 4.853; 95% CI, 1.124-20.952, P = 0.034) and preoperative hemoglobin level (OR: 0.624; 95% CI, 0.476-0.954, P = 0.026) were independent predictors of in-hospital mortality after CABG. CONCLUSION: Preoperative poor CCC and hemoglobin are predictors of in-hospital mortality after CABG with IABP support.

Effects of cilostazol on oxidative stress, systemic cytokine release, and spinal cord injury in a rat model of transient aortic occlusion.

BACKGROUND: Cilostazol is a phosphodiesterase inhibitor that has anti-inflammatory potential in addition to vasodilator and antiplatelet effects. The aim of this study was to determine the influence of cilostazol on biochemical markers of oxidative damage, proinflammatory cytokine release, and spinal cord injury after transient aortic occlusion in rats. METHODS: Animals were randomized into 3 groups. Sham group rats were subjected to laparotomy without aortic occlusion. Control group rats were pretreated with intraperitoneal dimethyl sulfoxide, and cilostazol group rats received intraperitoneal cilostazol (20 mg/kg/day) for 3 days before the induction of ischemia. Ischemia was induced by clamping of the infrarenal aorta, and 48 hours after reperfusion, Tarlov grades were assessed and spinal cord conduction velocities (SCCVs) were measured using epidural electrical stimulation. Erythrocyte superoxide dismutase (SOD) and catalase activities and plasma malondialdehyde, serum tumor necrosis factor-α, interleukin-1ß, and interleukin-6 levels were analyzed. Spinal cord histopathology was examined to determine neuronal damage and tissue inflammation. RESULTS: Aortic occlusion caused significant increases in SOD, catalase activities, and malondialdehyde and cytokine levels accompanied by spinal cord injury. Cilostazol significantly reduced malondialdehyde levels but did not significantly alter the activations of antioxidant enzymes, levels of proinflammatory cytokines, or histologic severity of inflammation. The differences regarding the results of Tarlov grading, SCCVs, and neuronal viability between the ischemic and cilostazol pretreated groups were statistically nonsignificant. CONCLUSION: The present experimental study indicated that cilostazol pretreatment used in this study before aortic occlusion decreased lipid peroxidation, which may be related to the reduction of reactive oxygen species. Cilostazol did not significantly suppress systemic cytokine release and prevent spinal cord inflammation and injury; however, it did show some benefit. Additional investigations might be needed to determine the critical dose of cilostazol for clarifying the protective role of this drug in spinal cord ischemia/reperfusion injury.

Spontaneous retrograde dissection of the ascending aorta in a patient with a bicuspid aortic valve.

Bicuspid aortic valve (BAV) is a congenital anomaly associated with structural weakness of the aortic wall. Sudden onset of symptoms in patients with BAV, such as sudden severe back pain, and pulse inequality between the extremities or tension disparity should alert clinicians to acute aortic syndromes, as they require prompt diagnosis and management. Retrograde aortic dissection, which is a rare form of acute aortic syndrome, is an uncommon life-threatening entity and may produce atypical computed tomography (CT) or magnetic resonance imaging findings, leading to difficulty in diagnosis. We report on a 51-year-old male patient with BAV and spontaneous retrograde ascending aortic dissection. CT findings were confusing and the diagnosis was made via transoesophageal echocardiography. After the diagnosis, the patient was treated with a modified Bentall procedure. He did not have any complications and was stable four months after the operation.

[Severe thrombosis of bioprosthesis mitral valve after dabigatran]. / Dabigatran sonrasi biyoprotez mitral kapakta ciddi tromboz.

A 41-year-old female was admitted to our hospital with an unidentified source of fever, dyspnea and dizziness. Transthoracic echocardiography demonstrated severe mitral valve regurgitation, and further examination with transesophageal echocardiography (TEE) revealed a 7 mm vegetation on the anterior mitral leaflet. Blood cultures were negative, and after 45 days of empiric 12 g/day ampicillin-sulbactam therapy, the vegetation was shown to have disappeared. However, due to ongoing severe mitral regurgitation and valve deformity, a prosthetic metallic mitral valve replacement was performed. After the operation, TEE was performed again due to subfebrile fever; however, the valve was normal and blood cultures were negative. Because of the probable relapse risk of infective endocarditis, the preoperative intravenous antibiotherapy was continued for 21 days and then orally for one week. Then, she was placed on follow-up by our outpatient clinic. As her INR was highly unstable during this period and she developed new-onset subfebrile fever, she was hospitalized again, and the TEE demonstrated vegetation. Blood cultures were still negative, and a combination of vancomycin-rifampicin-gentamicin was started. While under that therapy, first stroke and after a few days recurrent trans-ischemic attack developed, and the vegetation was seen to have enlarged. Urgent valve operation was performed with a bioprosthetic mitral valve, and ampicillin-sulbactam therapy was added to her previous antibiotherapy at the suggestion of the Microbiology Department. Oral anticoagulant therapy was planned for three months; however, during the postoperative period, her INR levels were highly unstable and could not be maintained in therapeutic ranges for even two consecutive days. Adjusted dosage of dabigatran to 110 mg/bid according to renal clearance in combination with 150 mg/day aspirin was started. However, valve thrombosis and a massive stroke developed under this therapy. The thrombosis disappeared after continuous heparin infusion, and she was discharged with neurological sequelae on 150 mg/day aspirin 55 days after her last operation. During the follow-up period of four months, no other clinical events occurred.

Preoperative poor coronary collateral circulation can predict the development of atrial fibrillation after coronary artery bypass graft surgery.

AIM: Coronary collateral circulation (CCC) helps to protect and preserve myocardium from episodes of ischemia, and reduce angina symptoms, arrhythmia, and cardiovascular events. Atrial fibrillation (AF) is the most frequent form of arrhythmia after coronary artery bypass graft (CABG) surgery. The aim of this study was to investigate the association between CCC and the development of AF in patients undergoing CABG surgery. METHODS: A total of 165 patients (mean age 63±10 years, 74% men, 26% women) who were undergoing CABG surgery at our department were enrolled into this study. Patients were categorized into two groups according to preoperative CCC using the Rentrop method. RESULTS: Of the patients, 79 had poor CCC and 89 had good CCC. The AF incidence rate in the poor collateral group was significantly higher than that in the good collateral group [37 (49%) vs. 12 (14%), P<0.001]. In univariate analysis, age, left atrium size, and poor CCC grade were associated with AF after CABG surgery. Multivariate analysis showed that only poor CCC grade (odds ratio: 11.500; 95% confidence interval 3.977-33.253, P<0.001) was an independent predictor of the development of AF after adjustment of other potential confounders in patients undergoing CABG surgery. CONCLUSION: The present study showed that preoperative poor CCC is a powerful predictor of the development of AF after CABG surgery.

Ozone therapy as an adjunct to vancomycin enhances bacterial elimination in methicillin resistant Staphylococcus aureus mediastinitis.

BACKGROUND: We aimed to investigate the influence of intraperitoneal ozone therapy on bacterial elimination and mediastinal inflammation in experimental Staphylococcus aureus mediastinitis. MATERIALS AND METHODS: Forty Wistar-Albino rats were randomized into five groups (eight per group) as follows: uncontaminated group, untreated contaminated group, ozone group, vancomycin group, and vancomycin + ozone group. Uncontaminated group underwent upper median sternotomy. The remaining four groups were inoculated with 0.5 mL 10(8) colony-forming units/mL methicillin-resistant Staphylococcus aureus in the mediastinal and sternal layers. Untreated contaminated group had no treatment. Rats in the vancomycin group received intramuscular vancomycin (40 mg/kg/d), and ozone was administered intraperitoneally (70 µg/mL, 1 mg/kg/d) in the ozone group for the treatment of mediastinitis. Vancomycin + ozone group rats were treated by the combination of both methods. At the end of 10 d, quantitative bacterial cultures and sternal tissue samples were obtained for determination of bacterial counts and histologic degree of inflammation. RESULTS: Both the vancomycin and the ozone treatments caused significant reduction of bacterial counts in quantitative bacterial cultures. Combination of vancomycin and ozone treatments resulted in further reduction of bacterial counts in mediastinum and sternum. Histologic examination of tissue samples revealed significant reduction in severity of mediastinitis related inflammation in vancomycin and vancomycin + ozone groups compared with untreated contaminated group. CONCLUSIONS: Ozone therapy as an adjunct to vancomycin leads to enhanced bacterial elimination in infected sternal and mediastinal tissues in experimental methicillin-resistant Staphylococcus aureus mediastinitis. The benefit of adjuvant ozone therapy is suggested to be related to its bactericidal effect.

Rupture of a pacemaker lead during the course of infective endocarditis.

A 23-year-old male who had a VDDR pacemaker implanted seven years ago due to sick sinus syndrome and recurrent syncope episodes was admitted with symptoms of dyspnea, fever, and tachycardia, which were present for a few days. He was suspected to be suffering from pneumonia and underwent computed tomography scanning of the thorax, which revealed widespread infiltration in the lung parenchyma and pulmonary emboli. Transthoracic echocardiography revealed an extremely mobile echogenic structure in the right atrium, which was determined to be the free portion of a ruptured pacemaker lead. There was an overlying thrombus and/or vegetation-like organized soft tissue within the right ventricle around the lead component. In this article, the rupture of a permanent pacemaker lead, which complicated the course of infective endocarditis associated with pulmonary embolism and pneumonia is reported. We hypothesize that the underlying mechanism for the rupture is soft tissue entrapment within the right ventricle. Unfortunately, this rare and life-threatening situation led to the death of our patient after the surgical removal of the device and its components.

Primary cardiac angiosarcoma with right coronary-to-right atrium fistula.

Primary tumours of the heart are rare. About 25% of all cardiac tumours are malignant and the most common of these is the angiosarcoma. We present a 61-year-old male with a right atrial angiosarcoma that was detected on coronary angiography. The tumour showed marked vascularity and a right coronary-to-right atrium fistula, and the patient underwent surgical resection. Pathological examination of the tumour was consistent with a cardiac angiosacoma and the diagnosis was also confirmed by immuno-histochemistry. He consequently underwent chemotherapy, however the patient died 60 days after the surgery.

Erdosteine ameliorates lung injury induced by transient aortic occlusion in rats.

The aim of this experimental study was to evaluate the protective effect of erdosteine on lung injury induced by ischaemia-reperfusion (IR) of the lower extremities of rats. Wistar albino rats (n = 21) were divided into three groups. In the IR group (n = 7), the aorta was cross-clamped for two hours, followed by one hour of reperfusion. In the erdosteine group (n = 7), animals were pretreated with erdosteine 100 mg/kg daily via gastric lavage, starting three days before aortic occlusion. In the control group (n 5 7), the lungs were removed and blood samples were taken immediately after sternotomy. No treatment was given in the control and IR groups. After both lungs were removed, biochemical parameters were measured and broncho-alveolar lavage (BAL ) assessment was made. MDA levels and MPO activities in the lung tissue were significantly reduced in the erdosteine group compared to the IR group. BAL assessment revealed decreased neutrophil counts in the erdosteine-treated group. Pretreatment of animals with erdosteine significantly attenuated transient aortic occlusion-induced remote lung injury, characterised by leukocyte accumulation and lipid peroxidation. The results suggest that erdosteine may be beneficial in amelioration of lung injury caused by IR.