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.

Association of Preoperative Platelet-to-Lymphocyte Ratio with Atrial Fibrillation after Coronary Artery Bypass Graft Surgery.

OBJECTIVE: The aim of this study was to investigate the association between platelet-to-lymphocyte ratio (PLR) and atrial fibrillation (AF) after coronary artery bypass graft (CABG) surgery. SUBJECTS AND METHODS: A total of 125 patients were retrospectively analyzed. AF was diagnosed using standard clinical criteria, and PLR was calculated as the ratio of the platelets to lymphocytes, obtained from the blood samples that were taken in the fasting state before CABG surgery. The association of different variables with postoperative AF and PLR was calculated using univariate and multivariate analysis. The receiver operating characteristics curve was used to determine the sensitivity and specificity of PLR and the optimal cutoff value for predicting post-CABG AF. RESULTS: Of the 125 patients, 50 with AF (mean age: 67.0 ± 9.5 years, 38 males and 12 females) and 75 patients without AF (mean age: 61.1 ± 9.1 years, 58 males and 17 females) were identified, and the difference in the mean age was statistically significant (p = 0.01). PLR was also significantly higher in those with AF (152.8 ± 82.2) than those without AF (118.2 ± 32.9) (p = 0.012). Univariate analysis showed that age and PLR were associated with AF after CABG surgery (p < 0.001 and p = 0.005, respectively). Using a multivariate logistic regression model with the backward elimination method, age and PLR remained as independent predictors of AF after CABG surgery (p < 0.001 and p = 0.005, respectively). PLR levels >119.3 predicted postoperative AF with 64% sensitivity and 56% specificity (AUC: 0.634, p = 0.012). CONCLUSION: In this study, age and PLR level were independent predictors of AF after CABG surgery. Patients with an elevated preoperative PLR were at higher risk of AF after CABG surgery.

Vascular pressure monitorization for necessity of vascular augmentation in a rat extended abdominal perforator flap model.

In case blood perfusion compromises, vascular enhancement with arterial supercharge or venous superdrainage can increase viability of the flap. In this study, vascular pressure monitorization was used in a rat extended abdominal perforator flap model to reveal intraoperative vascular compromise and the need for vascular augmentation. A rat abdominal perforator flap was designed, which was based on the right second cranial perforator of epigastric artery. Vascular pressures of the flap were monitored continuously for 60 min, by catheters placed in the right superficial inferior epigastric artery and vein. Forty rats were divided into four experimental groups, as follows: group 1 (n = 10, no vascular augmentation), group II (n = 10, arterial supercharge), group III (n = 10, venous superdrainage), and group IV (n = 10, arterial and venous augmentation). Arterial supercharge and/or venous superdrainage were performed by using the left superficial inferior epigastric artery and vein. After the rats were sacrificed on the 7th day, total flap area and necrotic regions were evaluated. Mean arterial blood pressure was found significantly lower (P < 0.05) and mean venous blood pressure was measured significantly higher (P < 0.05) in group I than the groups II, III, and IV. Flap survival area was also larger in the groups II, III, and IV than the group I (P < 0.05). The results of this experimental study demonstrate that arterial insufficiency and venous congestion are almost always present in the rat extended abdominal perforator flap model, similar to deep inferior epigastric perforator flap. When such an extended perforator flap is used, arterial and venous pressure monitorization may be considered as a tool to support intraoperative clinical findings to reveal the need of vascular augmentation and ascertain flap viability.