Aim: This study is aimed at validating the hypothesis that administration of cyclosporine-A (CsA) would be protective in lung ischemia-reperfusion (I/R) injury and in exploring the underlying mechanism. Methods: Rabbits were divided into 4 groups: the control, sham operation, I/R, and I/R with CsA treatment. Flow cytometry was used to measure the mitochondrial membrane potential. Laser scanning confocal microscope was used to analyze mitochondrion permeability transition pore (MPTP). The apoptotic cell was detected by the TUNEL staining. Western blot was performed to analyze the protein expression levels. Results: CsA not only attenuated the histopathologic alterations in lung and mitochondria after I/R injury, but also attenuated I/R injury through increasing MPP and inhibiting MPTP opening. Besides, CsA attenuated I/R injury through suppressing the release of cytochrome-c (CytC), inhibiting cell apoptosis and decreasing the expression levels of cyclophilin-D (Cyp-D), adenine nucleotide translocase 1 (ANT1) and voltage-dependent anion channel 1 (VDAC1). Finally, we found that Cyp-D knockdown inhibits I/R injury-induced MPTP opening and cell apoptosis. Conclusion: Our study found that the protective role of CsA on lung I/R injury depends on the inhibition of MPTP and CytC release, suppression of the activation of mitochondrial apoptosis pathway and the expressions of apoptotic-related proteins, as well as the decreased expression levels of ANT1 and VDAC1.
Although further study is required to assess the long-term function of the reconstructed tricuspid valve, our early and midterm results from this current study indicate that repairing the tricuspid valve with autologous pericardium achieves reasonable outcomes in the majority of patients with Ebstein's anomaly, including pediatric and adult patients.
BackgroundThe traditional approach for adult congenital heart disease combined with valvular disease is surgical treatment under cardiopulmonary bypass (CPB). This approach has a high incidence of postoperative complications, especially in patients with pulmonary hypertension and old age. We present two patients in whom the hybrid procedure was used to treat congenital malformations, followed by valve formation and replacement surgery.Case presentationA 63-year-old man had a muscular ventricular septal defect complicated by mitral regurgitation and a 57-year-old man had patent ductus arteriosus complicated by aortic stenosis. In both of the patients, the congenital malformation was successfully treated by the hybrid procedure, followed by valve repair or replacement. Both patients had no complications. A post-procedure echocardiogram showed no residual shunt across the duct.ConclusionsOur findings suggest that the hybrid procedure is a useful alternative for treating adult congenital heart disease with valvular heart disease. This procedure reduces the surgical incision and difficulty of surgery, shortens the CPB time, avoids residual leakage after surgery, and reduces recovery and hospitalization times.
Background: Obesity is associated with an augmented risk of myocardial ischemia/reperfusion (I/R) injury. Reduction of I/R injury by effective cardioprotective strategies needs to be investigated in obese subjects. This study aimed to evaluate the combined effects of sitagliptin and melatonin on inflammatory response and TLR4/IκBα/NF-κB signaling following cardiac I/R damage in obese rats. Methods: Sixty-six male Wistar rats (180–200 g) were fed a low fat diet (10% Kcal from lipids) or high fat (45% Kcal from lipids) diets for 12 weeks. High fat-fed (obese) rats experienced 30 min left anterior descending occlusion followed by 24 h reperfusion. Obese rats received sitagliptin (20 mg/kg/day) for 1 month before I/R surgery. Melatonin (10 mg/kg) was injected at early reperfusion. Myocardial infarct size (IS), cTn-I release, pro-inflammatory cytokines, myeloperoxidase (MPO), COX-2 and iNOS, and the protein expressions of TLR4, p-NF-κB/p65, and p-IκBα were evaluated. Results: Monotherapies with sitagliptin-preconditioning or melatonin-postconditioning had no cardioprotective effects in obese rats. However, combined therapy with sitagliptin and melatonin significantly reduced IS, and the release of cTn-I, in comparison to untreated obese rats ( p < .01) Moreover, this combination decreased the production of pro-inflammatory cytokines, MPO, COX-2 and iNOS, and the expression of TLR4 and p-NF-κB/p65, while reduced the expression of p-IκBα, in comparison with untreated or monotherapies-received obese rats ( p < .01 for all). Conclusion: Combination therapy with sitagliptin and melatonin was a good cardioprotective strategy to modulate the inflammatory responses and TLR4/NF-κB signaling pathway in obese patients with cardiac I/R injury.
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