Mehmet Fatih Alpay

Effect of topical N-acetylcysteine in the prevention of postoperative pericardial adhesion formation in a rabbit model.

BACKGROUND N-acetylcysteine (NAC), a precursor of reduced glutathione, has been in clinical use primarily as a mucolytic. In addition, NAC is well known for their free radical scavenging and antioxidant properties. Increasing of reactive oxygen products occurring during cardiac surgery can play an important role in postoperative adhesion formation. We investigated to the efficacy of the NAC for postoperative pericardial adhesions. METHODS Sixteen New Zealand white rabbits (2.5-3 kg) were used and categorized into two groups including study (use of NAC) and control groups. In both groups, the pericardium was opened longitudinally, and the exposed epicardial surfaces were abraded with dry gauze. The rabbits were divided into two groups: Group 1 was treated with the sponge, which impregnated with NAC solution, (10%, 300 mg/3 ml) and applied over the abraded epicardium for 5 min (n=8). Group 2 was the control, and the sponge, which was impregnated with 3-ml isotonic NaCl solution (0.9%), was applied onto the surface of the abraded epicardium for 5 min (n=8). After a period of 2 weeks, the animals were sacrificed. The scores of adhesion were graded by macroscopic examination, and the pericardial tissues were analyzed microscopically in point of inflammation and fibrosis. RESULTS In Group 1, the adhesion scores were significantly lower compared with the control group [Group 1 vs. 2; 1 (1-2) vs. 3 (2-3), P<.001]. No significant difference was found between the groups in terms of the severity of inflammation [Group 1 vs. 2; 1.5 (1-3) vs. 2.5 (1-3), P=.083]. There was a difference between groups in terms of the degree of fibrosis [Group 1 vs. 2; 2 (1-2) vs. 3 (2-3), P=.007]. CONCLUSIONS The use of NAC for preventing postoperative pericardial adhesions was reduced to adhesion and fibrosis scores in an experimental rabbit model. There was no statistically significant difference between groups in terms of inflammatory scores. The NAC effectively prevented the formation of pericardial adhesion.

Cilostazol Attenuates Spinal Cord Ischemia-Reperfusion Injury in Rabbits

OBJECTIVE The aim of this study was to evaluate the pretreatment effect of cilostazol on spinal cord ischemia-reperfusion injury. DESIGN Prospective, interventional study. SETTING Research laboratory, single institution. PARTICIPANTS Twenty-four New Zealand white rabbits. INTERVENTIONS Twenty-four rabbits were divided into 3 equal groups: group I (sham), group II (ischemia-reperfusion, control group), and group III (cilostazol, administered orally 30 mg/kg/day for 3 days before the surgery). Spinal cord ischemia was induced by clamping the aorta both below the left renal artery and above the iliac bifurcation for 30 minutes. Seventy-two hours postoperatively, the motor function of the lower limbs was evaluated in each animal according to the modified Tarlov score. Spinal cord and blood samples were taken for histopathologic and biochemical analyses at the 72nd hour of reperfusion. MEASUREMENTS AND MAIN RESULTS All rabbits in the ischemia-reperfusion group (group II) showed severe neurologic deficits. The median (IQR) Tarlov scores postoperatively at 72 hours in groups I, II, and III were 5.0(-), 2.0(1.0), and 4.5(1.0), respectively. Administration of cilostazol resulted in a significant reduction in motor dysfunction when compared with the ischemia-reperfusion group (p<0.001). In the ischemia-reperfusion group, serum and tissue glutathione peroxidase and superoxide dismutase activity were significantly less compared with the sham group (group I) (p<0.05). Serum and tissue glutathione peroxidase and superoxide dismutase levels in the cilostazol-treated group (group III) were higher compared with the ischemia-reperfusion group (p<0.05). In the cilostazol-treated group, serum and tissue malondialdehyde levels were lower compared with the ischemia-reperfusion group (p<0.05). Histopathologic analysis found decreased neuronal injury in the cilostazol group when compared with the ischemia-reperfusion group (p< 0.05). CONCLUSIONS This study showed that pretreatment with cilostazol significantly ameliorated neurologic functional outcome and attenuated neuronal histopathologic injury after transient aortic occlusion in rabbits.

Neuroprotective effect of atorvastatin in spinal cord ischemia-reperfusion injury

OBJECTIVES: Prevention of the development of paraplegia during the repair of the damage caused by descending thoracic and thoracoabdominal aneurysms remains an important issue. Therefore, we investigated the protective effect of atorvastatin on ischemia-induced spinal cord injury in a rabbit model. METHOD: Thirty-two rabbits were divided into the following four equally sized groups: group I (control), group II (ischemia-reperfusion), group III (atorvastatin treatment) and group IV (atorvastatin withdrawal). Spinal cord ischemia was induced by clamping the aorta both below the left renal artery and above the iliac bifurcation. Seventy-two hours postoperatively, the motor function of the lower limbs of each animal was evaluated according to the Tarlov score. Spinal cord and blood samples were obtained for histopathological and biochemical analyses. RESULTS: All of the rabbits in group II exhibited severe neurological deficits. Atorvastatin treatment (groups III and IV) significantly reduced the level of motor dysfunction. No significant differences were observed between the motor function scores of groups III and IV at the evaluated time points. Light microscopic examination of spinal cord tissue samples obtained at the 72nd hour of reperfusion indicated greater tissue preservation in groups III and IV than in group II. CONCLUSION: This study demonstrates the considerable neuroprotective effect of atorvastatin on the neurological, biochemical and histopathological status of rabbits with ischemia-induced spinal cord injury. Moreover, the acute withdrawal of atorvastatin therapy following the induction of spinal cord ischemia did not increase the neuronal damage in this rabbit model.

Assessment of the efficacy of Ankaferd blood stopper on the prevention of postoperative pericardial adhesions.

Summary Objectives Ankaferd has been used as a blood-stopping agent and it may also have an anti-inflammatory effect. We investigated the efficacy of Ankaferd in preventing postoperative pericardial adhesions in an experimental rabbit model. Methods Sixteen New Zealand white rabbits were used and categorised into two groups: an Ankaferd and a control group. The Ankaferd group of rabbits was treated with a sponge impregnated with Ankaferd solution, which was applied over the abraded epicardium. A sponge impregnated with 0.9% isotonic NaCl solution was applied to the control group using the same protocol. Scores for adhesion and visibility of coronary vessels were graded by macroscopic examination, and pericardial tissues were analysed microscopically in terms of inflammation and fibrosis. Results In the Ankaferd group, the adhesion scores were significantly higher than in the control group (p = 0.007). When the groups were compared according to the prevalence of fibrosis and degree of inflammation, the Ankaferd group was found to be statistically significantly different from the control group in terms of prevalence of fibrosis (p = 0.028). Conclusion Topical application of Ankaferd to prevent postoperative pericardial adhesions increased adhesion and fibrosis scores.

The Effect of Mitomycin-C in Reducing Pericardial Adhesion After Cardiac Surgery in Rabbits

BACKGROUND Mitomycin-C has been in clinical use primarily as a chemotherapeutic agent and is well known for antifibrotic properties. It has been widely used to prevent postoperative fibroblast proliferation and reduce scar adhesion in ophthalmologic and otolaryngologic operations. We investigated the efficacy of mitomycin-C in reducing postoperative pericardial adhesions in a rabbit model. METHODS New Zealand white rabbits were used and categorized into 2 groups, study (use of mitomycin-C) and control. Group 1 (n = 8) was treated with a sponge impregnated with mitomycin-C solution that was applied over the abraded epicardium. In group 2 (control group), the sponge was impregnated with 0.9% isotonic NaCl solution and was applied with the same protocol as the mitomycin-C-impregnated sponge in group 1 (n = 8). Rabbits were humanely killed at a mean of 2 weeks. The scores of adhesion were graded by macroscopic examination, and the pericardial tissues were analyzed microscopically in terms of inflammation and fibrosis. RESULTS In group 1, the adhesion scores were significantly lower than the control groups. No significant difference was found between the groups in terms of the severity of inflammation. There was a difference between groups in terms of the degree of fibrosis. CONCLUSIONS The use of mitomycin-C to prevent postoperative pericardial adhesions reduced adhesion and fibrosis scores in an experimental rabbit model. However, efficacy in reducing inflammation was not demonstrated.

A fatal complication after repair of post-infarction ventricular septal rupture: heparin-induced thrombocytopenia with thrombosis.

Abstract Heparin-induced thrombocytopenia (HIT) is a rare but potentially devastating and life-threatening complication from using heparin. HIT not only causes thrombocytopenia, but it also carries an increased risk for fatal thrombotic complications. In this report, we describe the case of a patient in whom fatal HIT developed after successful surgical repair of a posterior post-infarction ventricular septal rupture with cardiopulmonary bypass.

Free-floating thrombus of the carotid artery with a homozygous methylenetetrahydrofolate reductase gene mutation: a case report.

Free-floating thrombus (FFT) of the carotid artery is a rare condition of currently unknown etiology. We describe a symptomatic patient with an FFT in the left common carotid artery. A duplex ultrasonography scan showed the presence of a mobile floating thrombus moving in cyclical motion with the cardiac cycles in the left common carotid artery. During emergency surgery, an FFT was seen at this location and removed. No underlying wall defect was seen at the time of surgery. In a genetic screening test, TT homozygous for the methylenetetrahydrofolate reductase (MTHFR) C677T genetic polymorphisms was detected. The patient recovered uneventfully, with no neurogical events. Lifelong anticoagulant therapy was recommended. An aggressive surgical approach is recommended in the patient to prevent embolic episodes.

Surgical Treatment of Pulmonary Artery Leiomyosarcoma: A Good Survival Without Adjuvant Therapy

Primary pulmonary artery leiomyosarcoma is a rare tumor that can be misdiagnosed as acute or chronic pulmonary thromboembolic disease. In this report, we present a case of a 58-year-old woman initially diagnosed with chronic thromboembolic pulmonary disease, but who was later found to have pulmonary artery leiomyosarcoma. A complete mass resection was performed surgically. The definitive pathologic examination was consistent with pulmonary artery leiomyosarcoma. Although the patient did not receive adjuvant therapy after the surgery, she had a good outcome and was free of disease 8 months after surgery.

Aorto‐Left Ventricular Tunnel with Its Origin in the Left Sinus of Valsalva Associated with a Single Coronary Artery and Aortic Insufficiency in an Adult

Abstract  Aorto‐ventricular tunnel is a rare congenital anomaly, an abnormal paravalvular communication between the aorta and the left ventricle. We report successful surgical correction in a patient with aorto‐left ventricular tunnel associated with a single coronary artery and aortic insufficiency who had undergone surgical correction a year before. (J Card Surg 2011;26:437‐439)