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ABSTRACT: BACKGROUND: To summarize the diagnostic and therapeutic experiences on the patients who suffered abdominal complications after cardiovascular surgery with cardiopulmonary bypass(CPB). METHODS: A total of 2349 consecutive patients submitted to cardiovascular surgery with CPB in our hospital from Jan 2004 to Dec 2010 were involved. The clinical data of any abdominal complication, including its incidence, characters, relative risks, diagnostic measures, medical or surgical management and mortality, was retrospectively analyzed. RESULTS: Of all the patients, 33(1.4%) developed abdominal complications postoperatively, including 11(33.3%) cases of paralytic ileus, 9(27.3%) of gastrointestinal haemorrhage, 2(6.1%) of gastroduodenal ulcer perforation, 2(6.1%) of acute calculus cholecystitis, 3(9.1%) of acute acalculus cholecystitis, 4(12.1%) of hepatic dysfunction and 2(6.1%) of ischemia bowel diseases. Of the 33 patients, 26 (78.8%) accepted medical treatment and 7 (21.2%) underwent subsequent surgical intervention. There were 5(15.2%) deaths in this series, which was significantly higher than the overall mortality (2.7%). Positive history of peptic ulcer, advanced ages, bad heart function, preoperative IABP support, prolonged CPB time, low cardiac output and prolonged mechanical ventilation are the risk factors of abdominal complications. CONCLUSIONS: Abdominal complications after cardiovascular surgery with CPB have a low incidence but a higher mortality. Early detection and prompt appropriate intervention are essential for the outcome of the patients.
Journal of Cardiothoracic Surgery 10/2012; 7(1):108. · 1.19 Impact Factor
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ABSTRACT: Acute lung injury is a frequent complication after cardiopulmonary bypass (CPB). Recent studies have reported that NF-κB plays an important role in the pathogenesis of post-CPB pulmonary dysfunction. Several signaling pathways, including the TLR4 pathway, induce NF-κB leading to an inflammatory response. We designed this study to determine whether or not curcumin inhibits TLR4 and MyD88 protein levels and ameliorates lung inflammatory injury in a rat CPB model.
Sprague-Dawley rats were randomly divided into the following five groups (n = 12): sham; control (CPB); vehicle; low-dose curcumin (L-Cur); and high-dose curcumin (H-Cur). The percutaneous beating heart CPB model of rat was established. Animals were pretreated with a single intraperitoneal injection of vehicle, L-Cur (50 mg/kg), or H-Cur (200 mg/kg) 2 h prior to CPB. Blood were sampled at various time points, then lung tissues and bronchoalveolar lavage fluid were harvested 24 h after CPB.
CPB induced a marked increase in the concentrations of interleukin-8, tumor necrosis factor-α, and matrix metalloproteinase-9 in plasma, bronchoalveolar lavage fluid, and lung tissues (P < 0.05 versus sham group), whereas curcumin pretreatment reduced these inflammatory markers. Curcumin had effective inhibitory effects on the expression of TLR4, MyD88, and NF-κB in lung tissues 24 h post-CPB (P < 0.05 versus vehicle group). Administration of curcumin remarkably decreased the lung injury score (L-Cur versus vehicle group, P = 0.024; H-Cur versus vehicle group, P = 0.013).
Curcumin may be an alternative therapy for protecting CPB-induced lung injury by suppressing the expression of inflammatory cytokines. This anti-inflammatory effect of curcumin is partly related to the inhibition of TLR4, MyD88, and NF-κB.
Journal of Surgical Research 12/2010; 174(1):73-82. · 2.25 Impact Factor
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ABSTRACT: Temporarily pulmonary hilum clamping is available for the trauma surgeon to deal with serious pulmonary injuries, but the physiologic influence needs further evaluation. This study was to establish a temporary pulmonary hilum clamping model for thoracic damage-control surgery and determine the safety time latitude of this manipulation.
After anesthetized and catheter instrumented, the left pulmonary hilus of pigs were clamped with a urethral catheter after thoracotomy maintained for three different time period, 90 minutes (C90), 120 minutes (C120), and 150 minutes (C150), and then unclamped. Hemodynamic data were recorded and serum samples were collected for d-dimer detection and other hematology analysis, as well as 1 cm3 pulmonary tissue was obtained for histologic study before clamping, at the end of clamping, and at 0.5, 1, 1.5, 2, and 4 hours after unclamping.
There were 100% of C90, 83.3% of C120, and 33.3% of C150 pigs survived. Animals of C150 group suffered highest blood pressure and heart rate, respiratory index, pulmonary dynamic compliance, and cardiac output. Pulmonary vascular resistance, platelet count, and D-dimer showed minor significant changes between C90 and C120 groups, whereas a marked changes in C150 animals during the study. There were much more serious histologic changes in C150 group compared with C90 and C120 groups.
We established a pulmonary hilum clamping animal model for pulmonary damage investigation. It was determined that 120 minutes was the longest safety time for hilum clamping without lethal pulmonary injury in porcine.
The Journal of trauma 04/2010; 68(4):810-7. · 2.48 Impact Factor
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ABSTRACT: An experimental model of cardiopulmonary bypass in rats with pulmonary hypertension is necessary to understand underlying mechanisms and develop protective strategies. Male Sprague-Dawley rats were randomly divided into a sham group, cardiopulmonary bypass group, pulmonary hypertension group, and pulmonary hypertension with cardiopulmonary bypass group. Both groups with pulmonary hypertension received a subcutaneous injection of monocrotaline 60 mg x kg(-1) on day 0. Cardiopulmonary bypass was instituted in one of them 21 days later. The sham and pulmonary hypertension control groups underwent cannulation only. Cardiopulmonary bypass was conducted for 60 min at a flow rate of 100 mL x kg(-1) x min(-1). Hemodynamic investigations, blood gas analysis, interleukin-6, tumor necrosis factor-alpha, and survival studies were performed subsequently. Time-dependent increases of serum interleukin-6 and tumor necrosis factor-alpha were found after cardiopulmonary bypass in both groups. This model allows the study of multiple organ pathophysiological processes after cardiopulmonary bypass in rats with pulmonary hypertension, as well as the evaluation of possible protective strategies.
Asian cardiovascular & thoracic annals 07/2009; 17(3):285-90.
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ABSTRACT: To establish a temporary pulmonary hilum clamping model for thoracic damage control surgery, as well as to determine the safety time latitude of this manipulation.
Pigs were anaesthetised and instrumented with a thermodilution cardiac output catheter. The left pulmonary hilum was clamped with a urethral catheter after thoracotomy, maintained for three different time periods (n=6 for each group), 90min (C90), 120min (C120) and 150min (C150) and then unclamped. Haemodynamic data were recorded and the serum samples were collected for D-dimer detection and other haematological analysis. A 1-cm(3) pulmonary tissue of the left lower lobe was also obtained for histological study before clamping, at the end of clamping and at 0.5, 1, 1.5, 2 and 4h after unclamping.
Postoperative survival rate in each group of the pigs was as follows: 100% (all six) of C90, 83.3% (five of six) of C120, and 33.3% (two of six) of C150. Blood pressure (BP) and heart rate (HR) increased after clamping and gradually declined after unclamping. The animals of C150 group suffered highest BP and HR, respiratory index, pulmonary dynamic compliance and cardiac output. Platelet count showed no significant changes between the C90 and C120 groups, whereas a decline was noticed in the C150 group. Pulmonary vascular resistance increased significantly after pulmonary hilum clamping; when unclamped, there were minor changes in animals of C90 and C120 groups while there was a persistent elevation in the C150 group. An elevated D-dimer was detected in the C150 group, whereas it was normal in the C90 and C120 groups. There was significantly serious inflammatory cell infiltration, perivascular oedema and haemorrhagic infiltration in the C150 group compared with the C90 and C120 groups.
We established a pulmonary hilum clamping animal model for investigating pulmonary damage. By studying the haemodynamic and lung function changes of three different unilateral pulmonary hilum clamping time, it was determined that 120min was the longest safety time for hilum clamping without lethal pulmonary injury in porcine models.
Injury 07/2009; 40(9):956-62. · 1.98 Impact Factor
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ABSTRACT: Erythropoietin (Epo) was recently defined as an endogenous agent with more than hematopoietic functions. Previously we explored the potential of this agent to ameliorate lung ischemia-reperfusion (I/R) injury. The present study aims to determine the optimal dose and timing of administration for improving lung injury, and to further investigate the mechanisms by which Epo ameliorates lung I/R injury. The left lungs of Sprague-Dawley rats underwent 90 min ischemia and 120 min reperfusion. Firstly, animals in different groups were intraperitoneally injected with various doses of recombined human erythropoietin (rhEpo) 24 h prior to operation, 2 h prior to operation, or after the onset of reperfusion. Pulmonary myeloperoxidase (MPO) activity and malondialdehyde (MDA) content were evaluated. Treatment with 3 KU/kg rhEpo 2 h prior to operation was optimal for attenuating pulmonary MPO activity and MDA content. With such treatment, ultrastructural changes of pneumocytes were observed, and the pneumocyte apoptosis index was also determined by terminal dUTP nick-end labeling method. The plasma concentrations of tumor necrosis factor (TNF)-alpha and matrix metalloproteinase (MMP)-9 were evaluated by enzyme-linked immunosorbent assay, and pulmonary expression by immunohistochemistry. When pretreated with rhEpo, the pneumocyte ultrastructure was predominantly maintained and the pulmonary apoptosis index was markedly reduced. In comparison with untreated animals, in treated animals the plasma concentrations of TNF-alpha and MMP-9 were significantly decreased, and their expression in lung tissue was markedly reduced as well. The results indicated that Epo potently protected against lung I/R injury by inhibiting systemic and local expression of TNF-alpha and MMP-9.
European journal of pharmacology 12/2008; 602(2-3):406-12. · 2.59 Impact Factor
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ABSTRACT: Hepatic injury after cardiac surgery was considered to be a consequence of cardiopulmonary bypass (CPB). This study tested the hypothesis that melatonin could attenuate the hepatic injury in a rat CPB model. Male Sprague-Dawley rats were randomly divided into four groups: sham-operation group, control group (given an equal volume of vehicle), low dose melatonin (10 mg/kg) treated group and high dose melatonin (20 mg/kg) treated group. Blood samples were collected at the beginning, at the cessation of CPB, and at 30 min, 1, 2, 3 and 24 h post-operation. Liver samples were harvested at 24 h after operation. The serum indices of the liver enzymes and systemic inflammation, as well as oxidative stress indices and the Ca++-ATPase activity of liver tissues were determined. In the control animals, the indices of liver enzymes, tumor necrosis factor-alpha (TNF-alpha) increased after operation, and liver inducible nitric oxide synthase (iNOS), malondialdehyde (MDA), myeloperoxidase (MPO) increased as well. However, the activities of liver antioxidative enzymes and the concentration of glutathione (GSH) decreased remarkably. Results in melatonin group showed that melatonin reversed all the biochemical changes, but there was no significant difference between the melatonin-treated groups. In addition, histological findings further supported these results. All results indicated that application of exogenous melatonin during operation preserves liver function by reducing oxidative stress and the systemic inflammatory response.
European Journal of Pharmacology 03/2008; 580(3):416-24. · 2.52 Impact Factor
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ABSTRACT: Inflammatory response in the lungs is a well-known complication after cardiopulmonary bypass (CPB). The main aims of our study were to explore whether pretreatment with simvastatin would inhibit toll-like receptor 4 expression and suppress lung inflammatory response in a rat CPB model.
Male Sprague-Dawley rats were divided into four groups (n = 6 each): sham group; CPB (control group); CPB plus low-dose simvastatin (5 mg/kg daily [L-Sim group]); and CPB plus high-dose simvastatin (10 mg/kg daily [H-Sim group]). Blood samples were collected at the beginning and at the termination of CPB, and at 1, 2, 4, and 24 hours after operation. The bronchoalveolar lavage fluid and lungs were harvested 24 hours postoperatively.
The simvastatin-treated groups had significantly higher ratios of PaO(2)/FiO(2) and lower values of respiratory index than the control group. We observed that simvastatin reduced CPB-induced toll-like receptor 4 and nuclear factor-kappaB expressions in CPB groups (p < 0.01, versus control group). The levels of interleukin-6, tumor necrosis factor-alpha, and monocyte chemotactic protein-1 in serum, bronchoalveolar lavage fluid, and lung tissues increased in CPB groups, whereas pretreatment with simvastatins reduced these inflammatory marks in a dose-dependent manner (p < 0.01, versus control group). Furthermore, pretreatment with simvastatin had a lower lung injury score (p < 0.05, versus control group).
These findings suggest that simvastatin inhibited CPB-induced toll-like receptor 4 upregulation and nuclear factor-kappaB activation, efficaciously reduing the pulmonary inflammatory response after CPB.
The Annals of thoracic surgery 12/2007; 84(6):2011-8. · 3.74 Impact Factor
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ABSTRACT: An increasing number of patients were undergoing cardiac surgery with cardiopulmonary bypass (CPB) and more attention had been paid to hepatic injury after CPB. This study was designed to test the hypothesis that melatonin and N-acetylcysteine (NAC) could attenuate hepatic injury induced by CPB in rats.
Male Sprague Dawley rats were randomly divided into four groups: sham, control (CPB + placebo), NAC (CPB + 250 mg/kg N-acetylcysteine), and melatonin (CPB + 20 mg/kg melatonin). Blood samples were collected at the beginning, at the end of CPB, and at 0.5, 1, 2, 3, and 24 h postoperation. Liver samples were harvested at 24 h after the operation.
In the control group, the levels of serum liver enzymes and tumor necrosis factor-alpha, activities of inducible nitric oxide synthase, malondialdehyde, and myeloperoxidase in liver tissue were significantly increased. In addition, swollen hepatocytes, vacuolization, and congestion in sinusoids were observed. These changes were markedly reversed in both NAC and melatonin groups. Furthermore, the glutathione content and liver antioxidative enzymes activities were significantly decreased in the control group compared with the sham group. However, the levels of these antioxidants were markedly elevated after NAC or melatonin treatment compared with placebo treatment.
Our findings showed that NAC and melatonin had acceptably beneficial effects against the CPB-induced hepatic injury.
Journal of Surgical Research 10/2007; 142(1):153-61. · 2.25 Impact Factor
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ABSTRACT: Oxidative stress and systemic inflammation response contribute to acute renal injury post cardiac surgery. We hypothesized that administration of the antioxidant N-acetylcysteine would be beneficial to renal function after cardiopulmonary bypass in a rat model.
Male Sprague-Dawley rats were divided into four groups (each n = 6): sham group, cardiopulmonary bypass group, and two N-acetylcysteine-treated cardiopulmonary bypass groups (bolus doses of 200 and 500 mg/kg in cardiopulmonary bypass prime). Blood samples were collected at the beginning of cardiopulmonary bypass, at the cessation of cardiopulmonary bypass, and at 2 and 12 postoperative hours. The kidneys were harvested at 12 postoperative hours.
Serum creatinine and cystatin C continuously increased in all cardiopulmonary bypass groups (P < .05 within groups). Tubular dilatation, tubular necrosis, and vacuole formation were found in epithelial cells in histomorphologic studies of the cardiopulmonary bypass groups, but N-acetylcysteine significantly reversed these effects (P < .05 between groups). Compared with the sham group, the reduced glutathione hormone content and the superoxide dismutase and catalase activities decreased in the cardiopulmonary bypass groups (P < .01). N-acetylcysteine-treated groups had higher levels of these antioxidants than the untreated bypass group (P < .05). Renal malondialdehyde, tumor necrosis factor alpha, and nuclear factor kappaB were notably increased in all cardiopulmonary bypass groups relative to the sham group (P < .01), and N-acetylcysteine attenuated these changes dose dependently.
Administration of the antioxidant N-acetylcysteine preserved renal function after cardiopulmonary bypass dose dependently. Furthermore, oxidative stress and systemic inflammation were significantly reduced in the treated animals.
The Journal of thoracic and cardiovascular surgery 04/2007; 133(3):696-703. · 3.41 Impact Factor
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ABSTRACT: Little is known about serum cystatin C as a marker of renal function in cardiac surgery patients. The aim of this study was to assess its utility post cardiopulmonary bypass (CPB).
60 heart valve replacement patients were enrolled, and 26 of them had low-dose corticosteroid treatment on the first 3 days postoperatively. Serum creatinine, serum cystatin C and 24-h creatinine clearance rate (CCR) adjusted by body surface area were determined preoperation, days 1, 2, 3, 7 post operation.
Serum creatinine increased and peaked at day 3 postoperatively, while cystatin C peaked at day 2, and the adjusted CCR also reached a minimum at day 2. The inverse of cystatin C correlated better with CCR than that of creatinine (r=0.751 vs. 0.629). Using adjusted CCR as "golden standard", cystatin C was superior to creatinine in diagnosing renal dysfunction (area under the curve [AUC] for cystatin C 0.876, 95% confidence interval 81.8-93.4; AUC for creatinine 0.801, 95% confidence interval 72.5-87.7; p=0.045). Low-dose corticosteroid treatment has no significant effect on cystatin C.
In agreement with many other investigators, the present findings support cystatin C is a reliable marker of renal function. It is superior to creatinine in patients post CPB.
Clinica Chimica Acta 01/2007; 374(1-2):116-21. · 2.54 Impact Factor
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ABSTRACT: Based on the findings that erythropoietin (EPO) has been proved to be a multiple functional cytokine to attenuate ischemia-reperfusion (I/R) injury in various organs such as brain, heart, and kidney in animals, this experiment was designed to evaluate the effect of pretreatment with recombined human erythropoietin (rhEPO) on I/R-induced lung injury.
Left lungs of rats underwent 90 min of ischemia and then were reperfused for up to 2 h. Animals were randomly divided into three experimental groups as sham group, I/R group, and rhEPO + I/R group (a single dose of rhEPO was injected intraperitoneally 3000 U/kg 24 h prior to operation). Lung injury was evaluated according to semi-quantitative analysis of microscopic changes, tissue polymorphonuclear neutrophils (PMNs) accumulation (myeloperoxidase (MPO) activity), and pulmonary microvascular permeability (Evan's blue dying method). Peripheral arterial and venous blood samples were obtained for blood-gas analysis after 5 min occlusion of right lung hilus at the end of reperfusion. The serum concentration of tumor necrosis factor (TNF)-alpha was also measured by the method of enzyme-linked immunosorbent assay.
Histological injury scoring revealed significantly lessened lung alveolus edema and neutrophils infiltration in the rhEPO pretreated group compared with I/R group (p < 0.05). The rhEPO pretreated animals exhibited markedly decreased lung microvascular permeability (p < 0.05) and myeloperoxidase activity (p < 0.05). Blood-gas analysis demonstrated that the pretreated animals had significantly ameliorated pulmonary oxygenation function (p < 0.05). The serum concentration of tumor necrosis factor-alpha in rhEPO pretreated group was markedly decreased compared with that of I/R group (p < 0.05).
Pretreatment with rhEPO appears to attenuate I/R-induced lung injury. This function is partly related with the capacity that rhEPO inhibits the accumulation of polymorphonuclear neutrophils in lung tissue and decreases the systematic expression of tumor necrosis factor-alpha.
European Journal of Cardio-Thoracic Surgery 06/2006; 29(6):902-7. · 2.55 Impact Factor
