Distinct age-adjusted D-dimer threshold to rule out acute pulmonary embolism in outpatients and inpatients.

INTRODUCTION: The diagnosis of acute pulmonary embolism (PE) is combinations of clinical probability assessments, plasma D-dimer (DD) test results, and/or computed tomographic pulmonary angiography (CTPA). OBJECTIVE: The aim of this study is to explore the appropriate DD cutoff using the immunoturbidimetric method in outpatients and inpatients. METHODS: We retrospectively enrolled 2689 patients with suspected PE between January 2014 and December 2019. All patients underwent clinical probability assessments, DD tests, and CTPA. We investigated the appropriate cutoff level for plasma DD tests in the correlation analysis and receiver operating characteristic (ROC) curves. RESULTS: Among all patients, 1263 were confirmed acute PE. The age-adjusted DD level was determined to be age × 10 µg/L (for patients aged >50 years) in outpatients. This cutoff value resulted in a sensitivity of 96.75% and a specificity of 87.02%, with the area under the curve (AUC) of 0.908 and the number needed to treat (NNT) of 1.18. For inpatients, the age-adjusted cutoff values for the biomarker DD demonstrated poor specificity (13.34%) and NNT (9.88). However, when the DD cutoff was adjusted to 2 × the upper limit of normal (ULN), the sensitivity increased to 93.19%, while the specificity remained at 29.55%, with the AUC of 0.610 and the NNT of 4.76. The optimal DD cut-off value was 3010 µg/L (about 5 × ULN), resulting in a sensitivity of 75.22% and specificity of 61.72%, with the AUC of 0.727 and the NNT of 2.7. CONCLUSION: Using the immunoturbidimetric method to measure DD, an age-adjusted DD cutoff (age × 10 µg/L, if aged >50 years) should be considered for outpatients with suspected PE. For inpatients, increasing the DD cutoff value to at least 2 × ULN yields the best test performance.

Prognosis assessment model based on low serum calcium in patients with acute pulmonary thromboembolism.

BACKGROUND AND OBJECTIVE: The pulmonary embolism severity index (PESI) and simplified PESI (sPESI) are recommended to recognize patients with acute pulmonary thromboembolism (PTE) with low prognosis risk, which is of great significance for treatment. This study aims to verify the influence of hypocalcaemia on the prognosis of patients with PTE and to establish a new prognosis assessment model. METHODS: This is an observational, multicentre study enrolling patients with PTE from February 2010 to June 2020 across 12 Chinese hospitals. Variables in PESI, serum calcium levels and patient survival status as of 5 July 2020 were collected. The area under the curve of the receiver operating characteristic curve, sensitivity, specificity and Youden index were used to evaluate model performance. RESULTS: In the cohort of 4196 patients with PTE, independent associations existed between hypocalcaemia and mid- and long-term mortalities (p <0.05). By including hypocalcaemia, the new 30-day death risk prediction rule, Peking Union Medical College Hospital rule (PUMCH rule), showed significantly higher specificity (0.622 [0.582, 0.661]; p <0.001) than the PESI (0.514 [0.473, 0.554]) and sPESI (0.484 [0.444, 0.525]) and similar sensitivity (0.963 [0.810, 0.999]; p = 0.161) with PESI (0.889 [0.708, 0.976]) and sPESI (0.963 [0.810, 0.999]) in the internal validation cohort. Well-performing predictive validity was also verified on a constructed external validation cohort. CONCLUSION: Hypocalcaemia is independently associated with mid- and long-term PTE mortalities. The PUMCH rule showed significantly higher specificity than the PESI and sPESI and similar sensitivity, which may be used as a prognostic assessment tool for patients with acute PTE.

Bronchial glomus tumor with calcification: A case report.

BACKGROUND: Glomus tumors (GTs), defined by modified smooth cells and normal glomus body cells, usually present with a small mass occurring in the soft tissue or dermis of an extremity, especially in the subungual region. However, other unusual sites, such as the respiratory tract, have also been reported. They are usually sporadic. Their imaging findings are usually nonspecific and likely to appear as a well-delineated round mass that usually lacks calcification. To our knowledge, we report the first case of bronchial GTs with calcification, reminding clinicians and radiologists that GT is one of the differential diagnoses when a calcified nodular mass is found. CASE SUMMARY: We report a case of a 33-yr-old Chinese man with cough and sputum for 11 d and hemoptysis for 5 d. Chest computed tomography revealed a calcified nodular lesion on the compressed posterior wall of the lower left main bronchus and bronchiectasis in the lower lobe of the left lung. To confirm the characteristics of calcified nodules, we performed fiberoptic bronchoscopy. The tumor tissue from the biopsy of bronchial mucosal lesions established the diagnosis of GT. Because the patient had no life-threatening symptoms, he was not treated with surgery. Clinical follow-up for 25 mo showed that the patient survived well without any discomfort. CONCLUSION: Bronchial GTs are usually not accompanied by calcification on computed tomography scans. To our knowledge, we report the first calcified bronchial GT. We recommend that clinicians consider GT as a possible differential diagnosis when a calcified mass of the bronchi is found.

[Lemierre syndrome caused by Arcanobacterium haemolyticum: a case report and review of the literature].

OBJECTIVE: To emphasize the importance of the early diagnosis and treatment of Lemierre syndrome caused by Arcanobacterium haemolyticum. METHOD: A case of Lemierre syndrome caused by Arcanobacterium haemolyticum and three similar reported cases were reviewed. RESULTS: A man complained of fever with a sore throat, and examination found an enlarged left tonsil with prominent exudate, normal blood routine test and chest radiograph. Although the patient received the treatment of penicillin G and azithromycin, his condition worsened. Blood test showed white blood cell count 13.59×10(9)/L (neutrophils 0.933), platelet count 7.4×10(9)/L, TBil 54.3 mmol/L, DBil 28.3 mmol/L, AST 127 IU/L, ALT 82 IU/L, serum albumin 19.3 g/L with the development of the conditions. Blood cultures grew Arcanobacterium haemolyticum and the piperacillin-tazobactam was administered until fever was controlled. In addition, anticoagulation was administered when the thrombus was confirmed in the left internal jugular vein. Two follow-up clinic visits over the following 4 months were unremarkable. Besides three similar cases reported, four patients were male, and the ages ranged from 19 to 54 years. The chief complaints were sore throat and fever (4/4), with neck pain (4/4). Physical examinations found pharyngitis (2/4), exudate or abscess in the tonsillar crypt (2/4), maculopapular rashes (2/4). Laboratory results showed leukocytosis and thrombocytopaenia (4/4), acute cholestatic liver dysfunction (3/4), acute renal failure (2/4), acute respiratory failure (1/4). The first chest radiographs were normal at the onset, but chest radiography features included peripheral nodules and cavitation (3/4), focal or wedge-shaped lesions (1/4), pleural effusion (1/4) with the development of the conditions. Blood culture proved that there was only growth of Arcanobacterium haemolyticum (2/4), both Fusobacterium necrophorum and Arcanobacterium haemolyticum were found (2/4). Amoxicillin/clavulanic acid or piperacillin/tazobactam was administered (4/4). Neck CT proved internal jugular vein thrombosis (3/4) and anticoagulation was administered (3/4). All patients recovered and no one died. CONCLUSIONS: The characters of Lemierre syndrome include primary oropharynx infection, septicaemia, septic or embolic phlebitis of jugular vein, and metastatic abscess. Early recognition and aggressive intravenous broad-spectrum antibiotics are critical to reduce mortality.

Varied response of the pulmonary arterial endothelium in a novel rat model of venous thromboembolism.

BACKGROUND: The experimental studies of venous thromboembolism (VTE) as an entity and the response of the pulmonary arterial endothelium after VTE are still rare. The objective of this study was to observe changes in the pulmonary arterial endothelium using a novel rat model of VTE. METHODS: Rats were allocated to the VTE (n = 54) or control groups (n = 9). The left femoral vein was blocked using a microvessel clip to form deep vein thrombosis (DVT). One, four or seven-day-old thrombi were injected into the right femoral vein to induce DVT-pulmonary thromboembolism (DVT-PTE). The rats were sacrificed 1, 4 or 7 days later (D(n(1,4,7)) P(n(1,4,7)) subgroups (n = 6)), and the lungs were examined using light and electron microscopy. RESULTS: On gross dissection, the rate of DVT formation was higher on day 1 (D(1)P(n): 100%, 18/18) than day 4 (D(4)P(n): 83%, 15/18; χ(2) = 5.900, P = 0.015) or day 7 (D(7)P(n): 44%, 8/18; χ(2) = 13.846, P = 0.000). On gross dissection, the positive emboli residue rate in the pulmonary arteries was lower in the D(1)P(n) subgroup (39%, 7/18) than the D(4)P(n) (73%, 11/15; χ(2) = 3.915, P = 0.048) and D(7)P(n) subgroups (100%, 8/8; χ(2) = 8.474, P = 0.004); however, light microscopy indicated the residual emboli rate was similar in all subgroups. Hyperplasia of the pulmonary arterial endothelium was observed 4 and 7 days after the injection of one-day-old or four-day-old thrombi. However, regions without pulmonary arterial endothelial cells and intra-elastic layers were observed one day after injection of seven-day-old thrombi. CONCLUSIONS: This novel model closely simulates the clinical situations of thrombus formation and is ideal to study pulmonary endothelial cell activation. The outcome of emboli and pulmonary arterial endothelial alterations are related to the age and nature of the thrombi.

Additive effect of tadalafil and simvastatin on monocrotaline-induced pulmonary hypertension rats.

OBJECTIVES: Tadalafil, an oral phosphodiesterase type-5 inhibitor, induces pulmonary vasorelaxation by inhibiting the breakdown of cyclic guanosine monophosphate whereas simvastatin, an oral 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase inhibitor, has been shown to reverse pulmonary hypertension (PH) and attenuate vascular remodeling in animal models of pulmonary hypertension. We investigated whether the combination of tadalafil and simvastatin, which has different mechanisms of action, is superior to either drug alone in a rat model of monocrotaline-induced PH. METHODS: Male Sprague-Dawley rats were randomized to gavage with a vehicle, tadalafil (10 mg/kg/day), simvastatin (2 mg/kg/day), or tadalafi + simvastatin 21 days after the monocrotaline (60 mg/kg) injections. The hemodynamic and histological changes in the pulmonary arterioles, right heart hypertrophy, interleukin 6 (IL-6) levels and perivascular inflammation in the lungs were measured 35 days after monocrotaline exposure. RESULTS: The combination of tadalafil and simvastatin showed significantly more improvement in the mean pulmonary hypertension pressure (mPAP) and right ventricular hypertrophy compared with each monotherapy (p < 0.05). Combination therapy had additive effects on the increases in lung IL-6 levels and the perivascular inflammation score. CONCLUSIONS: These results suggest that the combination of tadalafil and simvastatin bears promise as an approach to treat PH, especially PH associated with inflammation.

[Simvastatin prevents the development of pulmonary hypertension in the rats through reduction of inflammation].

OBJECTIVE: To investigate the protection of simvastatin on monocrotaline (MCT)-induce pulmonary hypertension (PH) and the mechanism thereof. METHODS: Thirty-two male Sprague-Dawley rats were randomly divided into 4 equal groups: PH group undergoing subcutaneous injection of MCT and then gastric infusion of normal saline (NS) once a day for 21 days, simvastatin control group undergoing subcutaneous injection of NS and then gastric infusion of simvastatin 2 microg/g once a day for 21 days, simvastatin intervention group undergoing subcutaneous injection of MTS and then gastric infusion of simvastatin 2 microg/g once a day for 21 days, and control group undergoing subcutaneous injection and gastric infusion of NS. Three weeks later the mean pulmonary arterial pressure (mPAP) was detected by right heart catheter. Then the rats were killed with their lungs taken out. Arterial wall area/vessel area (W/V), and arterial wall thickness/vessel external diameter (T/D) were calculated. Perivascular inflammation was scored with the subjective scale of 0 (no) to 4 (severe). Pulmonary interleukin (IL)-6, tumor necrosis factor alpha (TNF-alpha), and monocyte chemotactic protein 1 (MCP-1) were tested by ELISA. RESULTS: The mPAP of the simvastatin intervention group was (23 +/- 7) mm Hg, significantly lower than that of the PH group [(34 +/- 9) mm Hg, P < 0.05], but not significantly different from that of the normal control group [(20 +/- 4) mm Hg, P > 0.05]. The W/V and T/D of the simvastatin intervention group were 0.442 +/- 0.061 and 0.325 +/- 0.045 respectively, significantly lower than those of the PH group (0.560 +/- 0.086 and 0.368 +/- 0.055 respectively, P < 0.01 and P < 0.05). The perivascular inflammation score of the simvastatin intervention group was (2.19 +/- 0.81), significantly lower than that of the PH group (3.40 +/- 0.65, P < 0.05), and the IL-6, TNF-alpha, and MCP-1 levels of the simvastatin intervention group [(264 +/- 127), (179 +/- 91), and (697 +/- 211) pg/ml respectively] were all significantly lower than those of the PH group [(765 +/- 179), (447 +/- 86), (4428 +/- 757) pg/ml respectively, all P < 0.01]. CONCLUSION: The protective effects of simvastatin against MCT-induced PH may be associated with the inhibition of the perivascular inflammation and lung IL-6, TNF-alpha, and MCP-1 levels.

[Study on changes of thrombi and vessel intima in a rat venous thromboembolism model].

OBJECTIVE: To observe the changes of thrombi and vessel intima in a rat model of venous thromboembolism (VTE). METHODS: Seventy-eight SD rats were randomly divided into deep vein thrombosis (DVT) group (n = 18), deep vein thrombosis-pulmonary thromboembolism (DVT-PTE) group (n = 54) and control group (n = 6). Rats in DVT and DVT-PTE groups were undergoing local blocking of left femoral artery with micro vessel clip to cause DVT. One, 4, and 7 days later 6 rats from DVT group were killed with their femoral veins observed by light and electron microscopy. Rats in DVT-PTE group underwent injection of the thrombi from left femoral vein solution in normal saline into the right femoral vein 1, 4, and 7 days after DVT formation to establish model of DVT-PTE. The 6 rats of each subgroup [D(n (1, 4, 7))P(n (1, 4, 7)) subgroups] were killed 1, 4, and 7 days after DVT-PTE formation respectively with their lungs observed by light and electron microscopy. RESULTS: (1) On day 1 after DVT, the successful rate of DVT was 100%. The positive thrombus rate in femoral veins on gross is lower on day 7 after DVT [42% (10/24)] than that on day 1 after DVT (chi(2) = 19.765, P < 0.01). The successful rates of DVT-PTE model were 100% (18/18), 83% (15/18), 44% (8/18) in the D(1)P(n), D(4)P(n) and D(7)P(n) subgroups respectively. The successful rate of DVT-PTE model is lower in the D(7)P(n) subgroups than that in the D(1)P(n) (chi(2) = 13.846, P < 0.01) and D(4)P(n) (chi(2) = 5.900, P < 0.05) subgroups. (2) One, 4, and 7 days after DVT, there were reddish, mixed, and organized thrombi in femoral veins. The thrombi in pulmonary arteries caused by the 4 or 7 days thrombi of DVT showed lower dissolubility than that from one day thrombi of DVT. The positive thrombus rate in pulmonary arteries on gross is higher in the D(4)P(n) and D(7)P(n) subgroups [73% (11/15) and 100% (8/8)] than that in the D(1)P(n) subgroups [39% (7/18, chi(2) = 3.915, P < 0.05; chi(2) = 8.474, P < 0.01)]. The ratio of vessel wall area and total vessel increased in D(1)P(7), D(4)P(4), D(7)P(4) and D(7)P(7) subgroups compared to the control group (P = 0.03, 0.00, 0.00, 0.011, respectively). (3) The junctures of femoral venous endothelial cells were ruptured and the intra-elastic layers were exposed on the 1(st) day, then the endothelial cells and intra-elastic layers became to disappear on the 7(th) day. The hyperplasia of pulmonary arterial intimal were observed on the 4(th) or the 7(th) day after the thrombi in pulmonary arteries caused by the 1 or 4 days thrombi of DVT. However, pulmonary arterial endothelial cells and intra-elastic layers maybe disappear on the 1(st) day after the thrombi in pulmonary arteries caused by the 7 days thrombi of DVT. CONCLUSIONS: The age and nature of thrombi before the embolization are related to the outcome of emboli and pulmonary arterial intimal alterations. For intimal, there are the changes of hyperplasia, intra-elastic layers thickening and even disappearance in femoral veins and pulmonary arteries after VTE.

[Establishment of rat model of venous thromboembolism].

OBJECTIVE: To establish a rat model of venous thromboembolism (VTE). METHODS: One hundred and forty-four SD rats were randomly divided into 2 equal groups: VTE-A group, undergoing local blocking of left femoral artery with micro vessel clip to cause deep vein thrombosis (DVT), and VTE-B group undergoing local blocking of left femoral artery with micro vessel clip in addition of administration of thrombin slowly injected from the distal end of the femoral vein blocked by micro clip. The rate of swelling limbs was observed. One, 4, and 7 days later 6 rats from each group were killed with their femoral veins taken out to observe the thrombosis rate by light microscopy. Other 18 rats in each group underwent injection of the thrombi from left femoral vein solution in normal saline into the right femoral vein 1, 4, and 7 days after DVT formation to establish model of DVT-pulmonary thromboembolism (PTE). The 6 rats of each group [VTE-A-D(n)P(n) and VTE-B-D(n)P(n) groups] were killed 1, 4, and 7 days after DVT-PTE formation respectively with their lungs taken out to observe the rate of PTE by light microscopy. RESULTS: (1) On day 1 after DVT, the successful rate of DVT was 100% in both VTE-A and VTE-B groups, and the swelling limb rate of the VTE-B group was 37.5% (27/72), significantly higher than that of the VTE-A group [16.7% (12/72), P = 0.005]. On day 7 after DVT, the positive thrombus rate of the VTE-B group was 83.3% (20/24), significantly higher than that of the VTE-A group [41.7% (10/24), P = 0.003]. One, 4, and 7 days after DVT, there were reddish, mixed, and organized thrombi in both VTE-A and VTE-B groups. (2) Tachypnea and tachycardia occurred immediately and disappeared spontaneously within 30 - 60 minutes when solution of thrombi was injected into pulmonary arteries via the right femoral veins. One rat died in the VTE-B-D(1)P(1) group 12 h after the embolization and was anatomically confirmed to suffer from fresh massive emboli lodged in pulmonary arteries. The successful rates of DVT-PTE model were 100% (18/18), 83.3% (15/18), and 44.4% (8/18) in the VTE-A-D(1)P(n), VTE-A-D(4)P(n), and VTE-A-D(7)P(n) groups respectively, and were 94.4% (17/18), 100% (18/18), and 83.3% (15/18) in the VTE-B-D(1)P(n), VTE-B-D(4)P(n), and VTE-B-D(7)P(n) groups respectively. The successful rate of DVT-PTE model in the VTE-B-D(7)P(n) group was higher than that in the VTE-A-D(7)P(n) group (P = 0.015). The thrombi in pulmonary arteries caused by the 4 or 7 days thrombi of DVT showed lower dissolubility in both VTE-A and VTE-B groups. CONCLUSIONS: A new rat model of VTE (DVT-PTE) has been successfully established. The successful rate of VTE can be increased when thrombin is slowly injected from the distal end of femoral vein blocked by micro clip in addition.

[The clinical analysis of pulmonary arterial hypertension in connective tissue disease].

OBJECTIVE: To investigate the clinical features and prognosis of pulmonary arterial hypertension (PAH) secondary to connective tissue disease (CTD). METHODS: Eighty-two patients diagnosed as having CTD associated PAH (CTDaPAH) were retrospectively analyzed among 2189 patients with CTD in Peking Union Medical College Hospital between January 1997 and September 2004. RESULTS: Eighty-two (3.7%) patients (75 females and 7 males), aged 41 years, were found to have CTDaPAH. The underlying diseases included mixed CTD (MCTD), systemic scleroderma, primary Sjogren's syndrome (pSS), systemic lupus erythematosus (SLE), undifferentiated CTD, dermatomyositis and Behcet disease. PAH was an earlier complication in patients with SLE or MCTD (median onset, 3 and 2 years, respectively), compared to those with pSS (6 years). The most common clinical manifestations of CTDaPAH were dyspnea on exertion (84.1%) and Raynaud's phenomenon (56.1%). The mean pulmonary artery systolic pressure (PASP) level of these patients was (65.71 +/- 20.44) mm Hg, with the decrease of PaO2 and PaCO2 level [(70.37 +/- 15.02) mm Hg, (27.88 +/- 6.46) mm Hg, respectively]. The diffusing capacity of the lungs measured using carbon monoxide was decreased [D(L)CO pred% (51 +/- 14)%]. 13%, 32%, 29% and 8% of these patients were grouped to class I, II, III and IV, respectively, on NYHA functional classification. Although the patients received treatment for underlying CTD and traditional vasodilators, the condition of elevated PASP had not been improved with the exception of a marginal decrease of PASP in SLE patients [(76.47 +/- 18.20) mm Hg --> (69.08 +/- 20.77) mm Hg]. Thirteen (15.85%) patients died during an average of 4.33 years follow-up, compared to the mortality of those with non-CTDaPAH (2.75%, P < 0.01). Lower level of PaO2 [(58.51 +/- 16.16) mm Hg] and higher proportion of NYHA class III, IV [38.46% (5/13), 30.77% (4/13), respectively] were observed in death group compared to survivors [PaO2 (73.25 +/- 14.32) mm Hg; NYHA class III, IV 34.78% (24/69), 5.80% (4/69), respectively] (P < 0.01; P < 0.05; respectively). CONCLUSIONS: PAH is a common complication of CTDs, which occurs often in the forth year after initial CTD manifestations and is earlier in patients with SLE or MCTD, compared to those with pSS. The most common manifestations of CTDaPAH are dyspnea on exertion and Raynaud's phenomenon. CTDaPAH could be very severe, which will lead to lower level of PaO2 and more advanced NYHA classification, and therefore reduce the survival rate of the patients. Doppler echocardiography and lung function test are necessary to detect PAH early.

[The change of pulmonary surfactant associated protein A in acute pulmonary embolism].

OBJECTIVE: To study the changes of pulmonary surfactant associated protein A (SPA) of lung tissue in acute pulmonary embolism (PE). METHODS: Male SD rats were injected with medical gelfoam microspheres via jugular vein to induce the PE model. Thirty-two rats were randomized into four groups: a control group (n = 8) and three groups of embolism for 24 h (n = 8), 1 week (n = 8) and 2 weeks (n = 8), respectively. The rats were sacrificed at the time of 2 weeks, 24 h, 1 week and 2 weeks. Pulmonary artery pressure, heart rate and respiratory rate were measured by right heart catheterization and artery blood gas was analyzed at the time of sacrifice. Lung tissues were sliced and stained with HE to observe the embolism of pulmonary arteries. RT-PCR and Western blot were used to study the changes of SPA mRNA and SPA protein in lung tissues. RESULTS: In the embolism rats, the pulmonary arterial pressure (mm Hg) increased significantly; the mean pulmonary arterial pressures of the 4 groups were 14.2 +/- 4.1, 26.1 +/- 7.5, 26.1 +/- 6.8 and 29.0 +/- 8.2, respectively (P < 0.05). The heart rate (per/minute) also increased significantly, 415 +/- 15, 451 +/- 35, 463 +/- 29 and 446 +/- 14, respectively in the 4 groups (P < 0.05). The arterial partial pressure of oxygen (mm Hg) decreased significantly, 94.1 +/- 8.8, 80.5 +/- 5.8, 80.4 +/- 13.8 and 73.4 +/- 14.3, respectively in the 4 groups (P < 0.05). After 24 h of embolism, pulmonary arteries were shown to be embolized with gelfoam, and later the gelfoam was resolved at week 2. The expression of SPA mRNA and protein in lung tissues decreased significantly after embolism; the mRNA level was 1.43 +/- 0.51, 0.83 +/- 0.33, 0.91 +/- 0.33 and 0.87 +/- 0.35 respectively in the 4 groups (P < 0.05); the protein level was, 1.00 +/- 0.00, 0.44 +/- 0.18, 0.44 +/- 0.33, and 0.52 +/- 0.32, respectively (P < 0.05). CONCLUSION: The SPA level decreases significantly in acute pulmonary embolism, which may play an important role in hypoxemia in pulmonary embolism.

[Study of serum uric acid changes after experimental pulmonary thromboembolism in rats].

OBJECTIVE: To study the change in serum uric acid (UA) after acute pulmonary thromboembolism (PTE) in rats and its value on the diagnosis of PTE. METHODS: Sixty-four male Sprague-Dawley rats were randomly divided into PTE group (n=34) and control group (n=30). Experimental PTE was induced in 34 rats by injection of auto-blood clots into the jugular vein (4 rats died and 30 survived), and another group of 30 rats underwent sham operation. Serum UA, partial pressure of oxygen in artery (PaO(2)), mean pulmonary arterial pressure (mPAP) and right ventricular pressure (RVP) were monitored on 1,4,7,14 and 28 days (n=6 per time point) after the operation. Lung tissue was harvested for histologic analysis using hematoxylin and eosin (HE) staining. RESULTS: Local hemorrhage in alveoli and inflammatory cell infiltration in interstitial tissue could be found microscopically within 1 week after PTE. The alveolar structure recovered and inflammatory cells in interstitial tissue decreased 7 days after PTE. Serum UA was higher in PTE group during 1-7 days after operation than in sham group (all P<0.05). PaO(2) was depressed markedly on 1,4 and 7 days after PTE (P<0.05 or P<0.01), and serum UA was negatively correlated with PaO(2) (r=-0.638, P<0.001); Serum UA returned to baseline 1 week after PTE, along with improvement of PaO(2) and alveolar hemorrhages. mPAP and RVP were not elevated in both groups. CONCLUSION: Serum UA content increases after experimental PTE in rats, and it may serve as a potential indicator of the severity and efficacy of treatment of PTE, but its clinical value need to be investigated.