Anthracyclines can cause severe cardiac toxicity leading to heart failure. The aim of this study was to determine the effects of cardioprotective polyphenolic compound resveratrol (RES) and adipose-derived mesenchymal stem cells (ADMSCs) on cardiac tissue of rats treated with doxorubicin (DOX). Forty-two female and three male Wistar-Albino rats were included in the study. The study groups and the control groups were as follows: Group I: DOX; Group II: DOX + RES; Group III: DOX + ADMSCs; Group IV: DOX + RES + ADMSCs; Group V: Sham operation; and Group VI: normal saline. ADMSCs obtained from male rats were defined with stem cell markers [CD11b/c(-), CD45(-), CD90(+), CD44(+), and CD49(+)]. DOX 12 mg/kg intraperitoneally (i.p.) was injected as a single dose in female rats. Resveratrol 100 mg/kg was injected three times i.p. in Groups II and IV. ADMSCs 2 × 10(6) cells/kg/dose were labeled with bromodeoxyuridine (BrdU) and injected i.p. for a total of three times in Groups III and IV. When the study was terminated after 4 weeks, the beating hearts were connected to a Langendorff setup and records were obtained for 30 minutes. Histopathological, immunhistochemical, and immunofluorescent examination with H&E, Troponin I, and BrdU stains were also performed. Also, ADMSCs were demonstrated in the myocardium of transplanted rats. Left ventricle functions and myocardial histology demonstrated significant impairment in DOX only group compared to groups with ADMSCs (P < .05). We suggest that RES and ADMSCs were successful in the prevention and treatment of the doxorubicin cardiomyopathy in rats. The hypothetical mechanisms of regeneration are multiple, including cell differentiation and autocrine/paracrine effects of ADMSCs.

Objective: The aim of this study was to assess the surgical and histopathological hemostatic effects of topical Ankaferd blood stopper (ABS) on major arterial vessel injury related to elevated intra-arterial blood pressure in an experimental rabbit model. Materials and Methods: The study included 14 New Zealand rabbits. ABS was used to treat femoral artery puncture on 1 side in each animal and the other untreated side served as the control. Likewise, for abdominal aortic puncture, only 50% of the aortic injuries received topical liquid ABS and the others did not (control). The experiment was performed under conditions of normal arterial blood pressure and was repeated with a 50% increase in blood pressure. Histopathological analysis was performed in all of the studied animals. Results: Mean bleeding time in the control femoral arteries was 105.0±18.3 s, versus 51.4±9.8 s (p<0.05) in those treated with ABS. Mean blood loss from the punctured control femoral arteries was 5.0±1.5 mg and 1.6±0.4 mg from those treated with ABS (p<0.05). Histopathological examination of the damaged arterial structures showed that ABS induced red blood cell aggregates. Conclusion: ABS administered to experimental major arterial vessel injury reduced both bleeding time and blood loss under conditions of normal and elevated intra-arterial blood pressure. ABS-induced erythroid aggregation was prominent at the vascular tissue level. These findings will inform the design of future experimental and clinical studies on the anti-bleeding and vascular repairing effects of the novel hemostatic agent ABS. (Turk J Hematol 2011; 28: 206-12)

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Objective: The aim of this study was to assess the surgical and histopathological hemostatic effects of topical Ankaferd blood stopper (ABS) on major arterial vessel injury related to elevated intra-arterial blood pressure in an experimental rabbit model. Materials and Methods: The study included 14 New Zealand rabbits. ABS was used to treat femoral artery puncture on 1 side in each animal and the other untreated side served as the control. Likewise, for abdominal aortic puncture, only 50% of the aortic injuries received topical liquid ABS and the others did not (control). The experiment was performed under conditions of normal arterial blood pressure and was repeated with a 50% increase in blood pressure. Histopathological analysis was performed in all of the studied animals. Results: Mean bleeding time in the control femoral arteries was 105.0±18.3 s, versus 51.4±9.8 s (p<0.05) in those treated with ABS. Mean blood loss from the punctured control femoral arteries was 5.0±1.5 mg and 1.6±0.4 mg from those treated with ABS (p<0.05). Histopathological examination of the damaged arterial structures showed that ABS induced red blood cell aggregates. Conclusion: ABS administered to experimental major arterial vessel injury reduced both bleeding time and blood loss under conditions of normal and elevated intra-arterial blood pressure. ABS-induced erythroid aggregation was prominent at the vascular tissue level. These findings will inform the design of future experimental and clinical studies on the anti-bleeding and vascular repairing effects of the novel hemostatic agent ABS. (Turk J Hematol 2011; 28: 206-12)

A retrospective analysis was made of the records of 62 patients who underwent pericardiectomy over a ten year period (1985 to 1996) in our department. Primarily, 43 patients (69.4%) had tuberculosis, 16 patients (25.8%) were diagnosed as idiopathic or viral infection, 2 patients (3.2%) had a previous cardiac operation and 1 patient (1.6%) had a neoplasm. Eight patients were in New York Heart Association functional class I, 22 in class II, 24 in class III, and 8 in class IV. Pericardiectomy was performed through midline sternotomy in all cases; 2 required cardiopulmonary bypass. Subtotal pericardiectomy was performed, in which the phrenic nerves define the posterior extent of pericardial resection. Low cardiac output was present in 8 patients. The early mortality rate was 6.45% (4 patients). During the follow-up period, ranging from 1 to 7 years (mean 3.8 ± 1.42 years), there were 2 late deaths due to the right heart failure. One patient who underwent pericardiectomy after an open-heart operation showed recurrent pericardial constriction. We conclude that pericardiectomy using midline sternotomy with or without cardiopulmonary bypass can be performed with low mortality and can result in good long-term survival and improved functional capacity.

The frequencies of angiotensin-converting enzyme gene insertion/deletion, angiotensinogen-M253T, and angiotensin II type 1 receptor-A1166C polymorphisms were analyzed in 105 patients undergoing coronary artery bypass grafting (group 1) and a control group of 105 non-cardiac patients (group 2). Blood samples were obtained for biochemical analyses and DNA extraction. Genotyping was performed by polymerase-chain-reaction-based restriction analysis. According to the angiotensin-converting enzyme gene insertion/deletion polymorphism, 36.3% of patients in group 1 and 30.7% in group 2 were homozygous for the DD allele. This difference was not statistically significant. Angiotensin II type 1 receptor-A1166C genotype polymorphism was also not significantly different between the groups. The results showed the angiotensinogen-M235T polymorphism to be heterogenous. The MM homozygote frequency was significantly higher in controls (72.3%), whereas 80% of the TT homozygote frequency was in the surgical group ( p = 0.001). These results show that although there were no significant differences in angiotensin-converting enzyme gene insertion/deletion and angiotensin II type 1 receptor-A1166C genotype polymorphisms between the groups, angiotensinogen-M235T polymorphism of TT homozygote frequency was significantly associated with patients undergoing coronary artery bypass surgery.

Twelve animals (26+/-5 kg) were subjected to the study. In this experimental study, the authors used prostacyclin to inhibit the toxic metabolite release during protamine administration. Animals were divided into two equal groups. Six animals received prostacyclin (the prostacyclin group), and the other six animals did not receive any additional treatment (the control group). All cardiac output and biochemical measurements were evaluated at baseline; before cardiopulmonary bypass; and at 5, 30, and 60 minutes after protamine administration. The measured cardiac index showed that the hearts treated with prostacyclin had satisfactory preservation of left ventricular function. Metabolic and biochemical data showed that the tumor necrosis factor level was raised significantly in the control group (20.75+/-2.2 in the control group and 13.75+/-2.5 pg/mL in the prostacyclin group). Also, E and P selectin levels were elevated in the control group, but this change was less marked in the prostacyclin group. In addition, the intracellular adhesion molecule-1 (ICAM-1) level was significantly higher in the control group than in the prostacyclin group (9.26+/-2.13 in the control group and 5.13+/-1.66 ng/mL in the prostacyclin group). The authors observed that prostacyclin inhibited the toxic mediator release during heparin reversal with protamine. This inhibition is one way of protecting the myocardium reserves from protamine cardiotoxicity.

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