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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: Acute renal dysfunction is a frequent complication after cardiac surgery with cardiopulmonary bypass (CPB). This study was designed to evaluate the potential protective effect of melatonin on CPB-induced renal damage in a rat model. Forty male Sprague-Dawley rats were randomly divided into four groups: sham, control (CPB + placebo), low dose of melatonin (CPB + 10 mg/kg melatonin) and high dose of 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 hr postoperation. Serum creatinine and blood urea nitrogen levels were assayed. Rats were killed 24 hr after surgery, the histologic appearance of the kidney and malondialdehyde (MDA), myeloperoxidase (MPO), catalase (CAT) and superoxide dismutase (SOD) contents were determined. The expression levels of hemeoxygenase-1 (HO-1) protein and gene were determined using western blotting and real-time PCR, respectively. In the control group, CPB surgery significantly increased urea, creatinine levels in serum, MDA and MPO levels in tissues, while decreasing SOD and CAT activities in tissues. Histopathologic findings of the control group confirmed that there was renal impairment by cast formation and tubular necrosis in the tubular epithelium. These changes were markedly reversed in both low dose of melatonin and high dose of melatonin groups. Furthermore, HO-1 gene transcript and protein were significantly upregulated in the kidney tissues after melatonin treatment compared with the placebo treatment. Our findings show that melatonin was effective in preventing CPB-induced renal damage probably through its antioxidant function and upregulation of HO-1.
Journal of Pineal Research 05/2009; 46(3):248-54. · 5.79 Impact Factor
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ABSTRACT: Recent in vitro data suggested that n-3 fatty acids could inhibit the activation of PPAR gamma. This study was designed to test the hypothesis that fish oil ameliorates CAV development via activating PPAR gamma in an inbred rat model of heart transplantation. Animals were divided into four groups: isograft, control (CsA + vehicle), LFO-treated group (CsA + 0.3% v/w fish oil), and HFO-treated group (CsA + 0.6% v/w fish oil). CsA was administered at 1.5 mg/kg/day for two wk postoperatively. Recipients were treated with fish oil or vehicle daily for eight wk. The histopathological and immunohistochemical examination, activity of NF-kappaB and PPAR gamma, intragraft chemokine levels, and chemokine receptor expression were analyzed. Both LFO and HFO significantly decreased the CAV score, inhibited recruitment of T lymphocytes and macrophages, elevated the activity of PPAR gamma, inhibited the activity of NF-kappaB, reduced levels of intragraft MCP-1 and IP-10 as well as downregulated expression of chemokine receptors CCR2. CXCR3 expression was not affected. Our results demonstrated that fish oil might attenuate CAV development, possibly through activating PPAR gamma and subsequently inhibiting the NF-kappaB activation, the chemokines secretion, as well as the CCR2 expression.
Pediatric Transplantation 06/2008; 12(5):550-6. · 1.48 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 study how CPB could induce and aggravate the hepatic injury in a rat model. Male Sprague-Dawley rats were randomly divided into two groups (n=12): sham and CPB groups. Blood samples were collected at the beginning, at the cessation of CPB, and at 0.5, 1, 2, 3 and 24 h post-operation. Liver samples were harvested at 24 h after operation. In CPB 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. On the contrary, the activities of liver antioxidative enzymes and the concentration of glutathione (GSH) decreased remarkably. All results indicated that CPB would induce and aggravate hepatic injury by facilitating oxidative stress and the systemic inflammatory response.
Interactive cardiovascular and thoracic surgery 03/2008; 7(1):18-22.
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ABSTRACT: RASSF1A is a novel putative tumor suppressor gene located in 3p21.3 region. The most common inactivation mechanism of RASSF1A is promoter hypermethylation, which is observed in multiple solid tumors including lung cancer. In the present study, we identified the methylation status of RASSF1A in lung cancer sera using methylation-specific PCR and analyzed its clinicopathological significance. Hypermethylation of RASSF1A was detected in 27 of 80 (33.8%) cancer patients but no benign pulmonary disease patients or healthy donors (P<0.001). RASSF1A hypermethylation was preferentially observed in small cell lung cancer (P=0.042), while no statistical difference was found among methylation frequencies of different subtypes of non-small cell lung cancer. RASSF1A methylation status was associated with differentiation (P=0.009) and stage (P=0.013), but not with gender, age or treatment. These findings suggest that serum RASSF1A hypermethylation is a promising molecular biomarker for lung cancer diagnosis.
Lung Cancer 05/2007; 56(2):289-94. · 3.43 Impact Factor
