RESUMO
Objective:To improve the understanding of the relationship between lymphedema and retroperitoneal fibrosis (RPF).Methods:Four cases with lymphedema and RPF in Beijing Shijitan Hospital Capital Medical University were reported. The diagnosis and treatment were analyzed and discussed.Results:All four patients had lymphedema onset and imaging showed suspicious RPF. One case of non-Hodgkin's lymphoma was confirmed by lymph node biopsy. The malignant lesions were excluded in the other two cases by pathology or positron emission tomography (PET)/computerized tomography (CT). They were proved to be idiopathic retroperitoneal fibrosis after treatment with glucocorticoid combined immunosuppressive agents. Another case was systemic amyloidosis mimicking retroperitoneal fibrosis.Conclusion:Lymphatic involvement in RPF is relatively rare, and the possibility of RPF should be considered when patients develop lymphedema. Even if the initial diagnosis is RPF, we should be wary of tumors or other diseases. Imaging examination should be performed, and tissue biopsy should be used if necessary, so as to facilitate early diagnosis and treatment and improve the prognosis of patients.
RESUMO
Objective:To observe the effect of annexin A1 peptidomimetic Ac2-26 on lung injury in rats with cardiopulmonary bypass, and analysis its anti-inflammatory mechanism.Methods:Eighteen male SD rats were divided into 3 groups(n=6) according to the random number table: sham operation group(S group), ischemia reperfusion group(IR group), Ac2-26 group(A group). The sham operation group received femoral arteriovenous puncture and catheterization, only the left lung was opened and the cardiopulmonary bypass tube was not connected. The other two groups were established with cardiopulmonary bypass left lung ischemia-reperfusion injury model. The IR group was given the same volume 10 minutes before cardiopulmonary bypass with the normal saline solution. Group A was injected with Ac2-26(1 mg/kg) through the tail vein 10 minutes before cardiopulmonary bypass. The arterial blood of the three groups of rats was taken for blood gas analysis before CPB(T1), immediately after opening the left lung hilum(T2), and at the end of the experiment(T3) to calculate OI and RI. At T1 and T3, the femoral vein blood was taken to measure the number of PMN. At T3, pulmonary artery blood was taken to measure the number of PMN and VCAM-1 content, left lung tissue was taken to measure NE and MPO content by ELISA, lung tissue neutrophil apoptosis was measured by Tunel method, and lung tissue ICAM-1 and AnxA1 protein expression was measured by Western-Blot.Results:At T3, compared with group S, the number of PMN in peripheral blood and pulmonary artery blood and the content of pulmonary artery VCAM-1 in IR group were significantly higher, the content of MPO and NE in lung tissue increased, the lung tissue pathological damage score increased, OI decreased and RI increased, all P<0.05. Compared with IR group, the lung tissue pathological damage score of rats in group A was significantly reduced, the number of PMN in peripheral blood and pulmonary artery blood and the content of VCAM-1 in pulmonary artery blood were significantly reduced, the expression of AnxA1 and ICAM-1 in the lung tissue of rats decreased; the content of MPO and NE in lung tissue decreased, and the apoptosis rate of PMN increased, all P<0.05. Conclusion:Ac2-26 annexin A1 peptidomimetics can inhibit the aggregation of neutrophils in the lung, weaken the adhesion of neutrophils to the pulmonary vascular endothelium, promote the apoptosis of neutrophils in the lungs, and reduce the content of NE and MPO. It has a protective effect on lung injury after cardiopulmonary bypass in rats.
RESUMO
Objective To evaluate the effect of dexmedetomidine on cell apoptosis during lung is-chemia-reperfusion(I/R)injury in a rat model of cardiopulmonary bypass(CPB).Methods Ninety-six SPF healthy adult male Sprague-Dawley rats,weighing 350-500 g,were divided into 4 groups(n＝24 each)using a random number table method: sham operation group(group S),CPB group(group C),CPB plus left lung I/R group(group IR),and CPB plus left lung I/R plus dexmedetomidine group(group D).The chest was only opened,and the rats underwent no CPB in group S.Only the CPB model was es-tablished in group C.The model of left lung I/R injury was established based on the CPB model in group IR.In group D,the model of CPB plus left pulmonary I/R injury was established,dexmedetomidine was intrave-nously infused in a dose of 3 μg/kg through the tail vein,followed by a continuous infusion of 1.5 μg?kg-1?h-1 until the end of surgery.Eight rats were selected in each group before operation(T0),at 10 min after opening the left hilum(T1),and at the end of operation(T2),the left lung tissues were taken for examination of pathological changes(with a light microscope)which were scored and for determination of cell apoptosis,and immunohistochemistry score(IHS)was assessed.The apoptosis index was calculated.Results Compared with group S,the pathological changes of lung tissues,IHS and apoptosis index were significantly increased at T1,2 in the other three groups(P＜0.05).Compared with group C,the pathologi-cal changes of lung tissues,IHS and apoptosis index were significantly increased at T1,2 in IR and D groups(P＜0.05).Compared with group IR,the pathological changes of lung tissues,IHS and apoptosis index were significantly decreased at T2 in group D(P＜0.05).Conclusion The mechanism by which dexme-detomidine reduces lung I/R injury during CPB is related to inhibiting cell apoptosis in rats.
RESUMO
Objective@#To evaluate the effect of dexmedetomidine on cell apoptosis during lung ischemia-reperfusion (I/R) injury in a rat model of cardiopulmonary bypass (CPB).@*Methods@#Ninety-six SPF healthy adult male Sprague-Dawley rats, weighing 350-500 g, were divided into 4 groups (n=24 each) using a random number table method: sham operation group(group S), CPB group(group C), CPB plus left lung I/R group (group IR), and CPB plus left lung I/R plus dexmedetomidine group (group D). The chest was only opened, and the rats underwent no CPB in group S. Only the CPB model was established in group C. The model of left lung I/R injury was established based on the CPB model in group IR.In group D, the model of CPB plus left pulmonary I/R injury was established, dexmedetomidine was intravenously infused in a dose of 3 μg/kg through the tail vein, followed by a continuous infusion of 1.5 μg·kg-1·h-1 until the end of surgery.Eight rats were selected in each group before operation (T0), at 10 min after opening the left hilum (T1), and at the end of operation (T2), the left lung tissues were taken for examination of pathological changes (with a light microscope) which were scored and for determination of cell apoptosis, and immunohistochemistry score (IHS) was assessed.The apoptosis index was calculated.@*Results@#Compared with group S, the pathological changes of lung tissues, IHS and apoptosis index were significantly increased at T1, 2 in the other three groups (P<0.05). Compared with group C, the pathological changes of lung tissues, IHS and apoptosis index were significantly increased at T1, 2 in IR and D groups (P<0.05). Compared with group IR, the pathological changes of lung tissues, IHS and apoptosis index were significantly decreased at T2 in group D (P<0.05).@*Conclusion@#The mechanism by which dexmedetomidine reduces lung I/R injury during CPB is related to inhibiting cell apoptosis in rats.
RESUMO
Objective To investigate the effect of lung ischemic preconditioning (IP) on the expression of aquaporin-1 (AQP1) during lung ischemia-reperfusion (I/R) induced by cardiopulmonary bypass (CPB) in dogs.Methods Twelve adult mongrel dogs,weighing 15-20 kg,were randomly divided into 2 groups (n =6 each):lung I/R (group I/R) and ischemic preconditioning group (group IP).The left pulmonary artery was occluded at 10 min of off-pump CPB and mechanical ventilation was stopped in the left lung,60 min later occlusion was released,and mechanical ventilation was recovered to establish the model of left lung ischemia-reperfusion injury induced by CPB.In group IP,lung ischemic preconditioning was induced by 2 cycles of 5 min ischemia followed by 5 min reperfusion before occlusion of the left pulmonary artery.Before CPB (T1),immediately after occlusion of the left pulmonary artery (T2),at the end of CPB (T3),and at 2 h after the end of CPB (T4),pulmonary specimens were collected for determination of wet to dry lung weight ratio (W/D ratio) and expression of AQP1 and for examination of the pathological changes of lungs which were scored.Respiration index (RI),oxygenation index (OI),and alveolar-arterial oxygen tension difference (P(A-a)O2) were calculated at T1,T3 and T4,and the left pulmonary alveolar fluid clearance (AFC) was calculated at T4.Results Compared with group I/R,P(A-a) O2 and RI were significantly decreased,OI was increased,W/D ratio and pathological scores were decreased,the expression of AQP1 was up-regulated,and the AFC was increased at T3 and T4 in group IP.The pathological changes of the lung were significantly attenuated in group IP as compared with group I/R.Conclusion The mechanism by which lung ischemic preconditioning mitigates lung I/R injury induced by CPB is related to upregulation of the expression of AQP1 in dog lung tissues.
RESUMO
Objective:To define the expression levels of MDM2 gene in nasopharyngeal carcinoma (NPC)and its relationship with p53 protein expression and EB virus latent infection. Method :MDM2 gene expression atmRNA and protein levels,p53 protein and EB virus DNA were detected by nonradioactive in situ hybridization(ISH) ,immunohistochemistry(IHC) and polymerase chain reaction (PCR) separately in 46 cases of NPC tissuesand 12 cases of chronic inflammation of nasopharyngeal epithelium (CINE). Result: Fourteen cases of NPCshowed MDM2 mRNA and protein overexpression, 38 cases were p53 protein positive,and 43 cases were EBV-DNA positive. Neither MDM2 nor p53 protein was expressed in any case of CINE. MDM2 expression was signifi-cantly related to p53 protein expression ( P ＜0. 05), but not to EB virus latent infection in NPC. Conclusion:MDM2 gene may play an important role in the pathogenesis of NPC through interacting with p53 protein.