[Assessment of meteorological conditions in relation to the onset of spontaneous pneumothorax in young adults].

Thirty-eight patients less than 30-year-old with spontaneous pneumothorax, of which onset date were known between January 2001 and December 2007, were included in this study. Meteorological factors such as temperature, humidity, atmospheric pressure, amount of rainfall and actual sunshine duration were assessed for the onset days of spontaneous pneumothorax (SP days) compared with days without pneumothorax (non-SP days) in the analyzed periods. The difference of those meteorological factors between the index day and one day before were also assessed. No significant difference was found in meteorological factors between SP and non-SP days. While, significant change in minimal temperature between SP days and non-SP days was found (+1.000 degrees C vs -0.015 degrees C, p=0.019). Meteorological factors may affect the onset of spontaneous pneumothorax in young adults. However, further assessment of accumulation of the patients is necessary including multi-institute study.

Neutrophil elastase inhibitor, sivelestat, attenuates acute lung injury after cardiopulmonary bypass in the rabbit endotoxemia model.

BACKGROUND: Neutrophil elastase probably contributes to the development of acute lung injury after cardiopulmonary bypass (CPB) in patients with infection or shock. We evaluated whether pretreatment with sivelestat sodium hydrate, a neutrophil elastase inhibitor (EI), can prevent acute lung injury caused by CPB. METHODS: Rabbits were assigned four groups: CPB for 60 minutes, control CPB group; low-dose lipopolysaccharide (LPS) administration without CPB, LPS group; CPB after lipopolysaccharide administration, LPS+CPB group; or preparation with continuous infusion of sivelestat and CPBs after lipopolysaccharide administration, EI group. Blood samples to determine blood gas concentration, plasma elastase activity, and plasma interleukin-8 levels were obtained. Histopathologic examinations of the lung were performed. RESULTS: The decreased arterial oxygen pressure at the end of CPB was observed in the LPS+CPB group only, but was suppressed in the EI group (p < 0.01). Elastase activity was markedly elevated at 120 minutes after CPB, and interleukin-8 levels were markedly elevated at 180 minutes in the LPS+CPB group but were much lower (p < 0.05) in the EI group. Histopathology demonstrated accumulation of polymorphonuclear neutrophils in bronchoalveolar areas in the LPS+CPB group (p < 0.01). Pulmonary myeloperoxidase activity was significantly lower in the LPS+CPB group than in the other groups (p < 0.01). These changes were minimal in the EI group. CONCLUSIONS: The combination of low dose LPS+60 minutes of CPB, but neither intervention alone, produced evidence of acute lung injury in a rabbit model. This did not occur when the animals were pretreated with sivelestat.

Design of a new technique using a free tracheal autologous graft for reconstruction of the cricoid cartilage and trachea.

PURPOSE: We devised a new operative procedure to recreate a supporting framework using a free tracheal autologous graft for cricoidal and tracheal defects. METHODS: We used this new transplantation method to repair the airway defect in five patients who underwent total thyroidectomy with resection of the airway for advanced thyroid cancer. A free graft was taken from the anterior aspect of the trachea and placed over the defect. The surface of the transplanted graft was then surrounded by the adjoining muscle flap. The orifice created by taking the graft was used as a temporary tracheostomy during the early postoperative period. RESULTS: Fiberscopic examinations and computed tomography scans done over 3-7 years postoperatively showed no airway deformity, subglottic stenosis, graft necrosis, or local recurrence in any of the five patients. The tracheal stoma closed spontaneously within 5 months after the operation in three of the five patients. CONCLUSION: The advantages of this procedure are: the free tracheal graft has as much strength as a prosthesis to support the respiratory tract; the autologous graft is biologically compatible; and the procedure can be completed in one surgical field and adopted for primary and secondary repair of the tracheal defect.

Platelet preservation with a glycoprotein IIb/IIIa inhibitor in a porcine cardiopulmonary bypass model.

BACKGROUND: We tested whether administration of FK633, a short-acting glycoprotein IIb/IIIa inhibitor, before median sternotomy and cardiopulmonary bypass was able to interrupt the platelet activation loop and thereby preserve platelet number and function. METHODS: This study investigated 16 pigs that underwent median sternotomy and 120 minutes of normothermic cardiopulmonary bypass (100 mL/kg) adding pericardial blood to the perfusate. FK633 was administered with heparin to one group (group F, n = 8), whereas only heparin was administered to the control group (group C, n = 8). Blood samples were obtained at several times, and complete blood count, platelet aggregation to adenosine diphosphate, thrombin-antithrombin complex, and bradykinin were evaluated. P-selectin expression and fibrinogen binding on platelet surfaces were measured by flow cytometry. Template bleeding times were measured before and after cardiopulmonary bypass. Chest tube drainage and hematocrit were determined at 2 and 6 hours after cardiopulmonary bypass. RESULTS: In group F, platelet counts were preserved from 90 minutes of cardiopulmonary bypass. Platelet aggregation was inhibited at the beginning of cardiopulmonary bypass and showed no change at wound closure, and bleeding times were shortened at 2 hours after cardiopulmonary bypass. There were significant reductions in hematocrit of drainage. Flow cytometry showed no changes in P-selectin expression and fibrinogen binding in group F, whereas P-selectin expression and fibrinogen binding were elevated in group C. CONCLUSIONS: Platelet inhibition with FK633 before invasive surgical procedure preserved platelet counts during and after cardiopulmonary bypass, and produced normal or near-normal bleeding times in the immediate postoperative period.

The state of platelets preserved in extracorporeal circulation with a glycoprotein IIb/IIIa inhibitor.

INTRODUCTION: Temporary inhibition of platelet function during extracorporeal circulation (platelet anesthesia) can preserve platelet count. We hypothesized that platelet anesthesia with a glycoprotein IIb/IIIa inhibitor could preserve activated platelets. MATERIALS AND METHODS: Fresh human blood from donors was recirculated for 120 min in a simulated extracorporeal circuit. Heparin and FK633, a short-acting platelet glycoprotein IIb/IIIa inhibitor, were added to recirculated blood in one group (group F, n=5) whereas only heparin was used in controls (group C, n=5). Blood samples were obtained from the donors, and at 0, 5, 15, 30, 60, and 120 min of recirculation. Platelet counts, beta-thromboglobulin, thrombin-antithrombin complex, and aggregation to adenosine diphosphate were measured. Flow cytometry was performed for measurement of fibrinogen binding, platelet surface expression of P-selectin, and microparticles. RESULTS AND CONCLUSIONS: In the FK633 group, platelet counts were preserved and beta-thromboglobulin levels remained unchanged, whereas in group C, platelet counts decreased significantly and beta-thromboglobulin increased significantly from 30 and 60 min, respectively. FK633 inhibited platelet aggregation and fibrinogen binding to platelets throughout recirculation. A significant difference between groups with respect to microparticle parameters and thrombin-antithrombin complex levels was evident by 120 min. P-selectin expression increased at 0 min in both groups, and was preserved significantly at 5 min and reduced at 120 min in group F. Platelet counts were preserved by platelet anesthesia during recirculation without platelet activation. These results suggest that FK633 inhibits the amplification loop by reducing the binding of fibrinogen to glycoprotein IIb/IIIa and platelet aggregation.

Surgical repair for chronic traumatic thoracic aneurysm after 12-year follow-up.

A 39-year-old man underwent surgical repair of chronic traumatic thoracic aneurysm after 12-year follow-up at our hospital. Eighteen years prior to surgery, he had been involved in a traffic accident, suffering a left hemopneumothorax. Chronic traumatic thoracic aneurysm is extremely rare that few guidelines for surgical intervention exist for this disorder. However, it has been observed that all patients with new symptoms should be operated promptly, and that asymptomatic aneurysm detected over 2 years after the initial trauma can be monitored by careful follow-up pending symptomatic or radiologic change. The present case provides additional support for these strategies.