Effect of low-molecular-weight heparin and urokinase on pulmonary arteries involved in pulmonary embolism.

BACKGROUND: Pulmonary embolism (PE) is a common and often fatal disease. Early after pulmonary thromboembolism, inflammation and associated intimal hyperplasia occur within the pulmonary arteries, similar to what is observed with chronic thromboembolic pulmonary hypertension. This study tested the hypothesis that thrombolytic and anticoagulant agents would have anti-inflammatory effects or inhibit intimal hyperplasia of involved pulmonary arteries. METHODS: Seventy-two male New Zealand white rabbits were randomly divided into two groups (54 rabbits in the PE group and 18 in the sham group). Experimental PE was induced in 54 rabbits by femoral vein injection of autologous blood clots and confirmed with pulmonary angiography, and other 18 rabbits underwent sham operations. Fifty-four rabbits in the PE group were randomly divided into three groups: a control group (treated with normal saline), a low-molecular- weight heparin (LMWH) group (treated with LMWH), and a urokinase (UK) group (treated with UK). Arterial blood gas was analyzed at 2, 7, and 28 days (n = 6 per time point by random group division), then lung tissues were removed and were analyzed for pro-inflammatory cytokines and chemokines, and were stained for intimal hyperplasia. RESULTS: The overall survival of rabbits undergoing PE was 100%. PE distribution detected on digital signal angiography (DSA) and histopathology was shown in 67% of rabbits (36/54) in the bilateral low lobar pulmonary arteries (PAs). The results showed that alveolar-arterial partial pressure of oxygen (PO2) difference (PA-aO2) significantly increased and PO2 decreased in the control group compared with the sham group. Compared with controls, the UK group had a decreased level of PA-aO2 on day 2 (P < 0.05), however, there was no significant difference in the LMWH group. Compared with controls, the LMWH group had a decreased level of monocyte chemoattractant protein-1 (MCP-1) in affected tissue and serum samples on days 7 and 28 (P < 0.05), and the UK group had decreased levels on days 2 and 7 (P < 0.05). Compared with sham group, all PE groups had an increased level of interleukin-13 (IL-13) and transforming growth factor-ß (TGF-ß) in unaffected lung tissue samples at days 2 and 7. IL-13 in affected lung tissue in the LMWH group was decreased at all time points compared with controls (P < 0.05). However, TGF-ß in affected lung tissue of the LMWH and UK groups increased at day 28. There was less intimal hyperplasia in involved pulmonary arteries at days 7 and 28 in the LMWH group compared with controls; there was no statistical difference in the UK group compared with controls. CONCLUSIONS: UK treatment can rapidly improve the V/Q mismatch in PE and appears a short-term anti-inflammatory benefit. However, LMWH maybe inhibit the later local inflammatory reaction and reduce intimal hyperplasia.

[Hypereosinophilic syndrome initially presenting pulmonary embolism: a case report and review of the literature].

OBJECTIVE: To analyze clinical features of hypereosinophilic syndrome with multiple thrombosis and improve the understanding of eosinophilia resulting in thrombotic diseases. METHODS: " Eosinophils increased, thrombocytopenia, deep vein thrombosis", as the Chinese keywords, "hypereosinophilic, thrombocytopenia, deep vein thrombosis", as the English keywords and to retrieve the literature from Wanfang database and Pubmed database January 2002- January 2012, a total of 17 articles, 5 Chinese articles, 4 in English, exclude those 2 articles which do not clearly diagnosis, a total of 7 articles were included, reports 8 cases, including 5 male, 3 female, age ranged from 24 to 75, combine the characteristics of the cases which reported in these literatures and our case, to make a literature review. RESULTS: A male, 27 years old complains shortness of breath, chest pain and blood in the sputum, pulmonary embolism diagnosed by chest enhanced CT, while deep vein thrombosis was diagnosed, laboratory examinations showed that blood eosinophils and thrombocytopenia. According to the literature that eosinophils can damage the vascular endothelial cells, leading to multiple arterial and venous thrombosis, anticoagulation while glucocorticoid treatment is effective. CONCLUSIONS: As one of eosinophilia, hypereosinophilic syndrome can involve multiple organs and cause multiple thrombosis. Anticoagulation and corticosteroids can reduce eosinophil count and decrease its toxins which can injure vascular endothelial.

[High-fat diet induces pulmonary fibrosis in rats and inhibitory effects of N-acetylcysteine].

OBJECTIVE: To explore the relation between high-fat diet and pulmonary fibrosis and the inhibition of N-acetylcysteine (NAC) on lung tissue in rats. METHODS: Thirty Sprague Dawley (SD) male rats were randomly divided into control group (n = 10) on a quantitative control Lieber-DeCarli liquid diet, a high-fat diet group (n = 10) on a high fat-diet Lieber-DeCarli liquid diet and NAC group (n = 10) on NAC 300 mg×kg(-1)×d(-1). All rats were sacrificed 8 weeks later. The morphological changes and collagen deposition in lung tissue were observed by hematoxylin & eosin and Masson staining while the contents of glutathione (GSH) and hyaluronic acid (HA) measured through colorimetry and enzyme-linked immunosorbent assay. And the expression of transforming growth factor-ß1 (TGF-ß1) expression in lung tissue was detected through immunohistochemistry. RESULTS: There were variable degree of alveolar and alveolar septal infiltration of inflammatory cells. And more deposition of collagen fibers appeared at intervals of alveolar in high fat group. Similar pathological changes were found in NAC group, but the degree was lower than that of high-fat group. Compared to the control and NAC groups, the lung tissue content of GSH decreased (GSH: 0.11 ± 0.05 vs 0.19 ± 0.11, 0.22 ± 0.14 mg/g, both P < 0.05) while HA and TGF-ß1 increased in high-fat diet group (HA: 0.57 ± 0.06 vs 0.46 ± 0.04, 0.41 ± 0.04 mg/g; TGF-ß1: 24.6 ± 3.4 vs 16.8 ± 2.6, 11.7 ± 1.5, all P < 0.05). CONCLUSION: High-fat diet may induce pulmonary fibrosis in rats and NAC has inhibitory effects.

Idiopathic pulmonary vein thrombosis extending to left atrium: a case report with a literature review .

Pulmonary vein thrombosis is a rare disease and is usually represented as a complication of atrial fibrillation, pulmonary tumors, and lobectomy. Although it is a potentially life threatening condition, the venous disease is easy to misdiagnose because of the non-specific symptoms. In this article, we present a 30-year-old patient who suffered from pulmonary vein thrombosis without any causes. He was diagnosed with other pulmonary disorders till the thrombus within the pulmonary vein extended into the left atrium. Left atrium mass resection and a left lower lobectomy were undertaken with relative urgency. The postoperative course was uneventful. The patient received a long course of oral anticoagulant therapy.

[Eleven fatal cases with A H1N1 influenza in Tianjin].

OBJECTIVE: To describe the clinical characteristics of fatal cases with confirmed A H1N1 influenza so as to improve the diagnosis and treatment of this severe disease. METHODS: We retrospectively analyzed the medical records of 11 fatal cases with A H1N1 influenza in Tianjin between September 1 and November 4 2009. RESULTS: There were 6 males and 5 females with a median age of 25 (21 - 36) years old. Two cases were pregnant women and 3 patients suffered such concurrent disorders as dilated cardiomyopathy, multiple myeloma or atrophic gastritis. Over 3 lung fields were involved on chest imaging studies and the oxygenation index was less than 300 mm Hg at admission. The therapies of oseltamivir and methylprednisolone were administered and mechanical ventilation was initiated within 24 hours. Refractory hypoxemia and a higher level of lactate dehydrogenase were present during treatment. Pneumothorax or mediastinal emphysema occurred in 4 patients, acute renal failure in 1 and pneumopyothorax in 1. The culture of airway secretion at 3 - 7 days after mechanical ventilation showed Staphylococcus aureus in 4 patients and Aspergillus in 2. The progress of disease was so quick that the duration from onset of clinical symptoms to hospitalization was a median of 4 (3 - 6) days and the duration from onset of clinical symptoms to death a median of 12 days. CONCLUSION: The fatal cases with A H1N1 influenza in Tianjin occurred mostly in young individuals and pregnant women. This severe disease had a rapid progression. And bacterial co-infections were quite common. Refractory hypoxemia resulting in respiratory failure was the main mortality reason.

[The lung protection strategy under the support of extracorporeal membrane oxygenation in patients suffering from influenza A H1N1].

OBJECTIVE: To study the effect of extracorporeal membrane oxygenation (ECMO) in patients suffering from severe pneumonia complicating influenza A H1N1 by putting lungs in rest to protect the latter. METHODS: Five patients with severe pneumonia following influenza A H1N1 were treated with ECMO and different modes of mechanical ventilation at the same time. Two patients died, both of them received synchronized intermittent mandatory ventilation (SIMV) and bi-level positive airway pressure (BiPAP) modes, with airway pressure release ventilation (APRV) to control lung expansion with expansion pressure 40 cm H(2)O (1 cm H(2)O=0.098 kPa). In 3 survivors, the strategy of lung rest was performed by giving an optimized positive end expiratory pressure (PEEP) with an optimal compliance by gradually elevation of PEEP, and high-level pressure (Phigh) at 20 cm H(2)O by application of BiPAP mode. RESULTS: One patient died due to lung damage and repeated spontaneous pneumothorax and sepsis; 1 patient died due to multiple organ dysfunction syndrome. Three patients recovered after following the strategy of lung rest. CONCLUSION: When ECMO is used for severe pneumonia complicating influenza A H1N1, prognosis can be obviously improved, with decrease in the occurrence of lung damage through the protection strategy of lung rest.

[Severe pneumonia caused by Aeromonas veronii biovar sobria: a case report and review of the literature].

OBJECTIVE: To describe the clinical features of severe pneumonitis with Aeromonas veronii biovar sobria. METHOD: Case report and review of the related literatures. The clinical symptoms, laboratory tests, radiographic patterns, diagnosis, and therapeutic management of a case of severe pneumonia caused by A. veronii biovar sobria were described. RESULTS: The clinical symptoms of this patient included cough and sputum production with high fever, followed by acute respiratory distress symptom associated with septic shock. Progressive infiltration of lungs was evident in chest radiography, changes suggestive of interstitial pneumonia. Oxygenation was improved by mechanical ventilation and anti-shock therapy was administered. A. veronii biovar sobria was grown in three consecutive cultures of airway secretions by fiberoptic bronchoscopy. Mild interstitial inflammation was revealed by pathology of transbronchial lung biopsy specimens. The clinical symptoms and the chest infiltrates improved significantly after therapy with antibiotics and glucocorticoids. CONCLUSIONS: A. veronii biovar sobria, an intestinal bacterial pathogen, can cause severe pneumonia, which is often underestimated and inadequately understood. Appropriate antibiotics, glucocorticoids and nutritional support are effective treatments.