Scielo RSS <![CDATA[Acta Cirurgica Brasileira]]> vol. 34 num. 8 lang. pt <![CDATA[SciELO Logo]]> <![CDATA[Effect of miR-134 against myocardial hypoxia/reoxygenation injury by directly targeting NOS3 and regulating PI3K/Akt pathway]]> Abstract Purpose To reveal the function of miR-134 in myocardial ischemia. Methods Real-time PCR and western blotting were performed to measure the expression of miR-134, nitric oxide synthase 3 (NOS3) and apoptotic-associated proteins. Lactic dehydrogenase (LDH) assay, cell counting kit-8 (CCK-8), Hoechst 33342/PI double staining and flow cytometry assay were implemented in H9c2 cells, respectively. MiR-134 mimic/inhibitor was used to regulate miR-134 expression. Bioinformatic analysis and luciferase reporter assay were utilized to identify the interrelation between miR-134 and NOS3. Rescue experiments exhibited the role of NOS3. The involvement of PI3K/AKT was assessed by western blot analysis. Results MiR-134 was high regulated in the myocardial ischemia model, and miR-134 mimic/inhibitor transfection accelerated/impaired the speed of cell apoptosis and attenuated/exerted the cell proliferative prosperity induced by H/R regulating active status of PI3K/AKT signaling. LDH activity was also changed due to the different treatments. Moreover, miR-134 could target NOS3 directly and simultaneously attenuated the expression of NOS3. Co-transfection miR-134 inhibitor and pcDNA3.1-NOS3 highlighted the inhibitory effects of miR-134 on myocardial H/R injury. Conclusion This present work puts insights into the crucial effects of the miR-134/NOS3 axis in myocardial H/R injury, delivering a potential therapeutic technology in future. <![CDATA[Stereological analysis of elastic fibers of the corpus cavernosum of rats during the aging process]]> Abstract Purpose To evaluate changes in the quantity of elastic fibers in the corpora cavernosa of rats during the natural aging process, and to assess the degree of this change by determining volumetric density (Vv) at different ages via stereological analysis. Methods Forty-eight rats, raised under similar conditions, were subjected to the natural aging process and divided into four groups (G1 to G4), according to age at the time of penectomy (6, 9, 12, and 24 months, respectively). Histological sections of the middle segment of the penis were stained with Weigert’s resorcin-fuchsin, and the volumetric density (Vv) of elastic fibers of the corpora cavernosa were determined via stereological analysis. Results There were no statistically significant differences in Vv among groups G1, G2, and G3. These three groups were therefore considered as a single group. The mean Vv of this group showed a statistically significant reduction compared to that of G4 (0.16 vs. 0.11, p&lt;0.05). Conclusion Natural aging in rats was responsible for a reduction in volumetric density of elastic fibers of the corpora cavernosa (approximately 30% decrease in Vv) during senescence. <![CDATA[The effect of different flushing methods in a short peripheral catheter]]> Abstract Purpose To develop a rabbit model of a short peripheral catheter (SPC) and to observe the effects of different flushing methods on blood vessels. Methods Thirty rabbits were randomly divided into three groups (A, B, and C), with ten rabbits per group. In group A, we used pulsed flush; in group B, we used uniform flush; and no treatment was used in group C. Results We observed that a uniform flush reduced blockage, phlebitis, and exudation compared to a pulsed flush by visual observation. The histopathological examination found that the morphological changes in group A were more severe than in group B and C related to loss of venous endothelial cells, inflammatory cell infiltration, edema, epidermal and chondrocyte degeneration, except for the thrombosis on group B that was more serious than in group A, especially in the distal side of puncture points. The distal region of groups A and B had more inflammatory cell infiltration than the proximal region. Thrombosis was more severe in the distal region than in the proximal region in group B. Conclusions The uniform flush produced less damage to the vascular endothelium and surrounding tissues and was superior to the pulsed flush. However, the uniform flush is prone to thrombosis. <![CDATA[Effect of sevoflurane pretreatment in relieving liver ischemia/reperfusion-induced pulmonary and hepatic injury]]> Abstract Purpose To investigate the effect of sevoflurane preconditioning on ischemia/reperfusion (I/R)-induced pulmonary/hepatic injury Methods Fifty-one Wistar rats were randomly grouped into sham, I/R, and sevoflurane groups. After reperfusion, the structural change of the lung was measured by Smith score, the wet and dry weights (W/D) were determined, malondialdehyde (MDA) myeloperoxidase (MPO) content was determined colorimetrically and by fluorescence, respectively, and matrix metalloprotein-9 (MMP-9) mRNA was quantified by RT-PCR. Biopsy and morphological analyses were performed on liver tissue, activities of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were determined, and tumor necrosis factor-alpha (TNF-α) level was determined. Results The sham group showed no changes in tissue structure. Structural lesions in the sevoflurane and I/R groups were mild and severe, respectively. Smith score, W/D, MDA, MPO, and MMP mRNA showed the same trend, and were increased in the I/R group and recovered in the sevoflurane group, compared with the sham group (both P&lt;0.05). AST and ALT were significantly increased compared to the sham group (AST: 655±52.06 vs . 29±9.30 U/L; ALT: 693±75.56 vs . 37±6.71 U/L; P&lt;0.05). In the sevoflurane group, AST and ALT levels were significantly decreased (464±47.71 and 516±78.84 U/L; P&lt;0.001). TNF-α presented similar results. Conclusion The protection of lung and liver by sevoflurane may be mediated by inhibited leukocyte recruitment and MMP-9 secretion. <![CDATA[The effect of fibrin glue in preventing staple-line leak after sleeve gastrectomy. An experimental study in rats]]> Abstract Purpose To evaluate the effect of fibrin glue on staple-line leak after sleeve gastrectomy. Methods Fourteen adult wistar rats 300 gr were randomized into two groups: Control group (n=7) and study group (n=7). All the rats underwent sleeve gastrectomy using lineer stapler. In the study group, fibrin glue was used to reinforce the staple-line. The rats were sacrificed 7 days after surgery. The stomach was resected, submerged in saline and exposed to excess pressure to obtain a burst pressure value. The gastric staple line was evaluated histopathologically according to the Ehrlich Hunt scale. The results of the two groups were compared. Results The mean Ehrlich-Hunt scores for inflammation, fibroblastic activity and neo-angiogenesis were similar between the groups (p&gt;0.05). Collagen deposition was significantly higher in study group (3.42±0.53) when compared with control group (2.57±0.78) (p=0.035). The mean burst pressure was 137.8±8.5 mmHg for control group and 135.0±8.1 mmHg for study group (p=0.536). Conclusion Reinforcement of the staple-line with fibrin glue has no effect on the burst pressure after sleeve gastrectomy. More studies are needed to evaluate the precautions against leak after sleeve gastrectomy. <![CDATA[Effects of cyclosporine on ischemia-reperfusion injuries in rat kidneys. An experimental model]]> Abstract Purpose To assess Cyclosporine A (CsA) therapy at an intraperitoneal dose of 15 -1 in a rodent model of non-septic renal ischemia. Methods Twenty male Wistar rats were randomized to receive CsA therapy or none therapy before undergoing 30 minutes of renal ischemia followed by reperfusion. Additionally, 10 rats were randomized to undergo the same surgical procedure of the aforementioned animals with neither ischemia nor CsA therapy. Twelve hours after kidney ischemia, the left kidneys were evaluated for histological injury according to Park’s criteria. Serum creatinine (Cr), urea nitrogen (Ur) and sodium levels were obtained at different times of the experimental protocol. Results Rodents in the CsA group showed negative results (p&lt;0.05) in serum variables (Cr: 0.41±0.05mg/dL vs . 4.17±1.25mg/dL; Ur: 40.90±3.98mg/dL vs . 187.70±22.93mg/dL) even the non CsA or control group (Cr: 0.35±0.07mg/dL vs . 3.80±1.20mg/dL; Ur: 40.10±4.70mg/dL vs . 184.50±49.80mg/dL). The negative results were also verified in histological evaluation, CsA group had 50% in the very severe grade of lesion, 10% in the severe and 40% in the moderate to severe whereas the control group had 90% in the very severe grade. Conclusion CsA was incapable of preventing the deleterious effects of ischemia-reperfusion injury in rat kidneys. <![CDATA[Mitigating effect of tanshinone IIA on ventricular remodeling in rats with pressure overload-induced heart failure]]> Abstract Purpose To investigate the effect of tanshinone IIA (TIIA) on ventricular remodeling in rats with pressure overload-induced heart failure. Methods Pressure overload-induced heart failure model (abdominal aortic coarctation) was established in 40 rats, which were divided into model and 5, 10 and 20 mg/kg TIIA groups. Ten rats receiving laparotomy excepting abdominal aortic coarctation were enrolled in sham-operated group. The 5, 10 and 20 mg/kg TIIA groups were treated with 5, 10 and 20 mg/kg TIIA, respectively, for 8 weeks. Results Compared with model group, in 20 mg/kg TIIA group the left ventricular ejection fraction, left ventricular fractional shortening, left ventricular systolic pressure, ±maximum left ventricular pressure rising and dropping rate, and myocardial B-cell lymphoma-2 and cleaved cysteinyl aspartate specific proteinase-3 protein levels were increased, respectively (P&lt;0.05), and the left ventricular end diastolic diameter, left ventricular end systolic diameter, left ventricular end diastolic pressure, heart weight index, left ventricular weight index, serum B-type brain natriuretic peptide, interleukin 6 and C-reactive protein levels and myocardial B-cell lymphoma-2 associated X protein level were decreased, respectively (P&lt;0.05). Conclusion TIIA may alleviate ventricular remodeling in rats with pressure overload-induced heart failure heart by reducing inflammatory response and cardiomyocyte apoptosis.