BACKGROUND:Previous experiment has confirmed that the nitinol artificial esophagus is an artificial succedaneum which can be used for replacing an esophagus resected and rebuilding esophageal tube.
OBJECTIVE:To observe the tissue reaction of the neo-esophagus and the adjacent organs injury contacted with the nitinol artificial esophagus after replacement.
METHODS:Eight miniature pigs were selected and modeled by resection of a 70 mm segment of the thoracic esophagus. After modeling, the nitinol artificial esophagus was inserted into the proximal and distal end of the thoracic esophagus at an insert distance of about 10 mm. After that, the nitinol artificial esophagus with polyester connecting ring was sewed into the thoracic esophagus in a manner of ful-thickness anastomosis. After operation, the pigs were subjected to feeding regulation measures to control the shedding time of the artificial esophagus. Two model pigs were sacrificed for anatomical observation at 1, 2, 3, 4 months postoperatively, respectively. The tissue reaction during the neo-esophagus formed procedure and adjacent organs injury contacted with the nitinol artificial esophagus were observed.
RESULTS AND CONCLUSION:Al pigs survived without complications such as thoracic hemorrhage, pneumothorax, pyothorax, esophageal perforation and anastomotic leakage. The experimental animals with the nitinol artificial esophagus fixed in situ had no dysphagia for eating semisolids food (Bown’SⅡ). Autopsy findings showed that there was slight membrane-like adhesion between partial pleura and lung. No hydrothorax was found. The nitinol artificial esophagus was wrapped up by the neo-esophagus. There was slight membrane-like adhesion between the neo-esophagus and the adjacent organs such as the lung, aorta and esophageal mucosa. The esophageal mucosa covered the neo-esophageal entocoele from esophageal stumps to intermedius of neo-esophagus until completely covered. Histological findings of the neo-esophagus showed that in imbed cycle of the nitinol artificial esophagus the tissue reaction showed aseprtic inflammation reaction and foreign body reaction around the implant. These tissue reactions were most severe at 1 month after operation and thereafter relieved gradual y.

To explore the effects of Shenmai Injection (SMI), a compound traditional Chinese herbal medicine, on pharmacokinetics and serum concentration of digoxin when applied together with digoxin.

Objective:To evaluate the role of SphK1/S1P signaling pathway in adiponectin-induced restoration of attenuation of myocardial ischemia-reperfusion (I/R) injury by sevoflurane postconditioning in diabetic rats.Methods:Healthy clean-grade male Sprague-Dawley rats, aged 8-10 weeks, weighing 250-300 g, in which diabetes mellitus was induced by combination of high-fat and high-sucrose diet and intraperitoneal injection of 1% streptozotoein in citric acid buffer 40 mg/kg, were studied.Ninety rats with diabetes mellitus were divided into 6 groups ( n=15 each) using a random number table method: sham operation group (group Sham), group I/R, sevoflurane postconditioning group (group S), adiponectin preconditioning group (group A), adiponectin preconditioning+ sevoflurane postconditioning group (group AS) and adiponectin preconditioning+ K6PC-5 (a specific SphK1 activator)+ sevoflurane postconditioning group (group AKS). Myocardial I/R was induced by 30 min occlusion of anterior descending branch of left coronary artery followed by 120 min reperfusion.At 15 min before ischemia, recombinant adiponectin 5.0 μg/g was injected intraperitoneally in A, AS and AKS groups, and K6PC-5 1 μg/g was injected via the tail vein in group AKS.In S, AS and AKS groups, 2.5% sevoflurane was inhaled for 5 min starting from the onset of reperfusion.Blood samples from the internal jugular vein were collected at the end of reperfusion for determination of serum cardiac troponin I (cTnI) concentration (by enzyme-linked immunosorbent assay), percentage of myocardial infarct volume (by TTC staining) and expression of SphK1, S1P and phosphorylated NF-κB p65 (p-NF-κB p65) in myocardial tissues (by Western blot). Results:Compared with group Sham, the serum cTnI concentration and percentage of myocardial infarct volume were significantly increased, and expression of SphK1, S1P and p-NF-κB p65 in myocardial tissues was up-regulated in group I/R ( P<0.05). Compared with group I/R, no significant change was found in each parameter in group S ( P>0.05), and the serum cTnI concentration and percentage of myocardial infarct volume were significantly decreased, and expression of SphK1, S1P and p-NF-κB p65 in myocardial tissues was down-regulated in group A ( P<0.05). Compared with group S, the serum cTnI concentration and percentage of myocardial infarct volume were significantly decreased, and expression of SphK1, S1P and p-NF-κB p65 in myocardial tissues was down-regulated in group AS ( P<0.05). Compared with group AS, the serum cTnI concentration and percentage of myocardial infarct volume were significantly increased, and expression of SphK1, S1P and p-NF-κB p65 in myocardial tissues was up-regulated in group AKS ( P<0.05). Conclusion:SphK1/S1P signaling pathway is involved in adiponectin-induced restoration of attenuation of myocardial I/R injury by sevoflurane postconditioning in diabetic rats.