Upregulated miRNA-1236-3p in osteosarcoma inhibits cell proliferation and induces apoptosis via targeting KLF8.

OBJECTIVE: To elucidate the regulatory effect of miRNA-1236-3p on the cellular behaviors of osteosarcoma (OS) cells, and to provide novel hallmarks and therapeutic targets for the diagnosis, treatment, and prognosis of OS. PATIENTS AND METHODS: Relative level of miRNA-1236-3p in OS tissues and cell lines was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Regulatory effects of miRNA-1236-3p on the proliferative ability of HOS and U-2OS cells were evaluated by cell counting kit-8 (CCK-8) assay. Through flow cytometry, the potential influences of miRNA-1236-3p on cell cycle progression and apoptosis of OS cells were examined. Subsequently, the dual-luciferase reporter gene assay was conducted to explore the binding of KLF8 (Krüppel-like factor 8) to miRNA-1236-3p. Regulatory effects of KLF8 on cellular behaviors of OC cells were also evaluated. RESULTS: MiRNA-1236-3p was downregulated in OS tissues relative to controls. Meanwhile, miRNA-1236-3p was lowly expressed in OS with worse TNM stage or distant metastasis. The overexpression of miRNA-1236-3p in HOS and U-2OS cells suppressed the proliferative ability, arrested the cell cycle in the G0/G1 phase and induced apoptosis. Conversely, miRNA-1236-3p knockdown obtained the opposite trends. KLF8 was verified to bind to miRNA-1236-3p, and its expression was negatively regulated by miRNA-1236-3p in OS cells. A series of functional experiments displayed the oncogenic role of KLF8 in OS. CONCLUSIONS: MiRNA-1236-3p is downregulated in OS tissues and cell lines. The overexpression of miRNA-1236-3p suppresses the proliferative ability and induces apoptosis of OS cells via downregulating KLF8.

Study of the momentum-resolved plasmonic field energy of Bloch-like surface plasmon polaritons from periodic nanohole array.

The angular surface plasmon mediated fluorescence from a two-dimensional Au nanohole array has been studied by reflectivity spectroscopy and Fourier-space photoluminescence microscopy. By using the rate equation model and temporal coupled mode theory, we determine the momentum-dependent coupling rate of light emitters to (-1,0) Bloch-like surface plasmon polaritons (SPPs) in the first Brillouin zone. The rate increases gradually when the SPPs propagate away from the Γ-X direction and split into two at the Γ-M point where two coupled modes are formed. In addition, both the spectral density-of-states (SDOS) and the plasmonic field energy are found to govern the momentum dependence. We also examine the behavior of the field energy as a function of the SPP propagation direction and it agrees well with the finite-difference time-domain simulations, showing the energy plays a major role in controlling the angular emission intensity. Our results devise a new method in studying the momentum-dependent plasmonic field energy and they are expected to provide insight in directional emission from periodic arrays.

Determination of complex Hermitian and anti-Hermitian interaction constants from a coupled photonic system via coherent control.

By manipulating the relative amplitude and phase between two incoming lights, coherent control of photonic systems can be realized. Here, we show by temporal coupled mode theory and finite-difference time-domain simulation that a coupled system can be actively controlled to exhibit plenty of different spectral, angular, and excitation behaviors. Electromagnetically induced transparency-like and Fano spectral characteristics as well as strong beam steering have been observed. Remarkably, by selectively exciting the coupled modes, we have developed a new approach to determine the complex Hermitian and anti-Hermitian interaction constants. We find the constants are strongly geometric and material dependent and they are of importance in understanding the non-Hermitian physics arising from the dissipative, open coupled system.

Determination of the excitation rate of quantum dots mediated by momentum-resolved Bloch-like surface plasmon polaritons.

When light emitters are being placed in close proximity to a plasmonic system, not only the emission but also the excitation can be strongly enhanced and both yield the surface plasmon polariton (SPP) mediated fluorescence enhancement. Here, we combine the rate equation model and coupled mode theory to formulate the excitation rate of light emitters located on a periodic metallic array. The rate is expressed in terms of quantities that can be measured by angle- and polarization-resolved reflectivity and photoluminescence spectroscopy. As a demonstration, we have studied the excitation rate of CdSeTe quantum dots deposited on a 2D Au nanohole array as a function of the propagation direction of the (-1,0) Bloch-like SPPs. At the excitation wavelength of 633 nm, we find the rate remains almost constant at ~44 ps-1 regardless of the propagation direction of SPPs, which move from the Γ-X towards the Γ-M direction in the first Brillouin zone, and the crossing of the (-1,0) and (0,-1) SPPs along the Γ-M direction where two bright and dark modes are formed. The results are supported by the finite-difference time-domain simulations. We conclude the excitation rate is an intrinsic parameter and the enhanced excitation of the quantum dots arises entirely from field enhancement.

[Soft-tissue angiosarcoma with pulmonary metastases: case report and literature review].

Objective: To investigate the differential diagnosis between pulmonary metastases from soft-tissue angiosarcoma and primary pulmonary angiosarcoma. Methods: A case of soft-tissue angiosarcoma with pulmonary metastases was reported and related literatures were reviewed. Results: A 39 year-old man complaining of hemoptysis, cough, and sputum for 10 months was admitted to our hospital in September 2013. He was initially diagnosed as having primary pulmonary angiosarcoma after wedge-resection biopsy of the lung. After 22 months since onset, he felt discomfort in his leg, which led to the confirmative diagnosis of soft-tissue angiosarcoma of the leg with multiple pulmonary metastases by a full-body PET/CT scan and core needle biopsy of the leg. Twenty-three articles concerning primary pulmonary angiosarcoma with complete records of history, treatment and follow-up of patients were included in the literature review. A total of 26 patients were reported in these articles, including 18 males, 8 females, age 19-85 years, average (52±18) years. Primary pulmonary angiosarcoma was mainly manifested as single or multiple pulmonary nodules or masses, with or without ground glass opacity. In our case, chest CT showed multiple thin-wall cysts and ground glass opacities, and recurrent spontaneous pneumothorax, which had never been reported in literatures on primary pulmonary angiosarcoma. Conclusions: Pulmonary metastases from soft-tissue angiosarcoma differed from primary pulmonary lesions in terms of chest imaging, with the former usually showing thin-wall cysts and pneumothorax. A full-body PET-CT was essential for differential diagnosis between primary and metastatic pulmonary angiosarcoma.

Hybrid particle swarm global optimization algorithm for phase diversity phase retrieval.

The core problem of phase diversity phase retrieval (PDPR) is to find suitable optimization algorithms for wave-front sensing of different scales, especially for large-scale wavefront sensing. When dealing with large-scale wave-front sensing, existing gradient-based local optimization algorithms used in PDPR are easily trapped in local minimums near initial positions, and available global optimization algorithms possess low convergence efficiency. We construct a practicable optimization algorithm used in PDPR for large-scale wave-front sensing. This algorithm, named EPSO-BFGS, is a two-step hybrid global optimization algorithm based on the combination of evolutionary particle swarm optimization (EPSO) and the Broyden-Fletcher-Goldfarb-Shanno (BFGS) algorithm. Firstly, EPSO provides global search and obtains a rough global minimum position in limited search steps. Then, BFGS initialized by the rough global minimum position approaches the global minimum with high accuracy and fast convergence speed. Numerical examples testify to the feasibility and reliability of EPSO-BFGS for wave-front sensing of different scales. Two numerical cases also validate the ability of EPSO-BFGS for large-scale wave-front sensing. The effectiveness of EPSO-BFGS is further affirmed by performing a verification experiment.

Momentum-dependent group velocity of surface plasmon polaritons in two-dimensional metallic nanohole array.

We determine the momentum-dependent group velocities of ( ± 1,0) and (0, ± 1) Bloch-like surface plasmon polaritons (SPPs) in two-dimensional Au nanohole array by measuring their propagation lengths and decay lifetimes at different SPP propagation length via angle- and polarization-resolved reflectivity spectroscopy and real- and Fourier-space microscopy. We find the decay length and lifetime, as well as group velocity, are highly dependent on the propagation direction. In particular, close to the Γ-M direction where two SPPs begin to interfere, the group velocity decreases due to the increase of the standing wave character. More importantly, the two SPPs are strongly interacted with each other at the Γ-M direction, resulting in forming the dark and bright modes. We find the group velocity of the dark mode is higher that of the bright mode despite its higher quality factor, or longer decay lifetime. We attribute such difference to the distinct field symmetries of dark and bright modes, yielding different effective indices. While bright mode has fields mostly concentrated at the flat metal region to produce higher effective index and therefore lower velocity, the fields of the dark mode are located near the air hole, resulting in higher velocity.

[Risk factors of lung cancer complicated with symptomatic venous thromboembolism].

OBJECTIVE: To seek risk factors of VTE in patients with lung cancer through analysis of clinical features of patients with lung cancer complicated with venous thromboembolism (VTE). METHODS: Retrospective investigation was performed on patients diagnosed with lung cancer and with complete clinical data who were hospitalized in Peking University People's Hospital from January 1, 2010 to December 31, 2014. According to the presence of symptomatic VTE, patients were distributed into two groups, VTE group and control group. Patients' clinical data and laboratory parameters were collected. Single factor analysis was applied to compare the differences between the two groups. t test or nonparametric test was applied for intragroup comparison of measurement data, and chi-square test was applied for the comparison of counting information. Logistic regression analysis was applied to explore risk factors of venous thromboembolism. For VTE patients with this diagnosis when they were hospitalized, D-dimer and PT were obtained after the occurrence of VTE, so D-dimer and PT were eliminated in the multiple factors analysis. SPSS 13.0 statistical software was applied for statistical management and analysis. RESULTS: 548 patients with lung cancer were include in the investigation, with male 357, female 191, average age of (63.8±10.9) years old, 46 patients in VTE group and 502 patinets in control group. According to the results of single factor analysis in gender, age, tumor pathologic type, tumor stage, WBC, Hb, PLT, CEA, ALT, FIB, D-dimer, PT, APTT, PT-INR, the tumor stage (χ(2)=14.177), CEA (t=2.129) and Hb (t=-2.424) were risk factors for lung cancer patients complicated with venous thromboembolism. Logistic regression analysis showed that tumor stage was the independent risk factor of lung cancer complicated with venous thromboembolism (OR 2.058, 95%CI 1.307-3.238, P=0.002) , and CEA (r=0.395, P<0.001) and Hb (r=-0.144, P=0.001) were associated with lung cancer stage. The area under the curve formed by D-dimer predicting VTE was 0.825 (95%CI 0.751-0.900, P<0.001). CONCLUSION: Tumor stage is the only risk factor for lung cancer patients complicated with venous thromboembolism in the study. However, because this study is a retrospective study, other potential high risk factors causing VTE cannot be excluded.

Association of a let-7 KRAS rs712 polymorphism with the risk of breast cancer.

Breast cancer (BC) is a common malignancy affecting women, with increasing incidences of this disease in China every year. Recent studies have extensively investigated a single nucleotide polymorphism in the let-7 miRNA binding site of the 3'-untranslated region of KRAS mRNA. The aim of this study was to determine the genotype frequency of the KRAS rs712 polymorphism, and evaluate its effect on BC risk. This hospital-based case-control study comprised 228 patients with histologically confirmed BC and 251 healthy controls. The let-7a KRAS rs712 polymorphism was analyzed by polymerase chain reaction-restriction fragment length polymorphism. We observed no statistically significant association between BC risk and the let-7a KRAS rs712 polymorphism (GT vs GG, OR = 0.98, 95%CI = 0.66-1.46; TT vs GG, OR = 0.78, 95%CI = 0.28-2.21). However, the rs712 polymorphism was significantly associated with the N status of BC patients (GG vs GT/TT, OR = 0.52, 95%CI = 0.30- 0.92; G allele vs T allele, OR = 0.60, 95%CI = 0.37-0.97). We found no association between the let-7 rs712 polymorphism and BC risk. However, the let-7 rs712 G/T polymorphism was discovered to play a potential role in BC tumor metastasis; therefore, it may be employed as a new biomarker or therapy targeted towards resistant tumor metastasis.

Determination of the absorption and radiative decay rates of dark and bright plasmonic modes.

When two degenerate surface plasmon polariton (SPP) modes couple, in addition to the creation of plasmonic band gap, their respective decay rates are modified as well, resulting in the formation of a pair of dark and bright modes. We combine temporal coupled mode theory, finite-difference time-domain simulation, and angle- and polarization-resolved reflectivity spectroscopy to study the absorption and radiative decay rates of this pair in periodic system. One-dimensional metallic groove arrays are served as an example here. We find for arrays with small groove width, when approaching to the coupling of -1 and + 1 SPP modes, while the radiative decay rate of the high energy mode tends to become zero, the absorption rate decreases as well, forming a "cold" dark mode. At the same time, both the absorption and radiative decay rates of the low energy mode increase, yielding a "hot" bright mode. The situation is completely reversed when groove width increases, turning the high energy mode into a "cold" bright mode and vice versa for the low energy mode. We attribute such modifications to the interplay between the real and imaginary parts of the complex coupling constant, which are found to be highly geometry dependent. Further numerical simulations show the hybridized modes exhibits distinctive electric and magnetic field symmetries, giving rise to different surface charge distributions and Poynting vector profiles, which significantly affect the resulting absorption and radiation losses. Finally, we have measured the decay rates and the complex coupling constant of the hybridized modes and the experimental results are consistent with the analytic and numerical results.

Study of coupling efficiency of molecules to surface plasmon polaritons in surface-enhanced Raman scattering (SERS).

Studying the interaction between molecules and surface plasmon polaritons (SPPs) is of great important in understanding surface-enhanced Raman scattering (SERS). While it is known that SERS consists of excitation and emission enhancements, each of them is manifested by several sub-steps which individually also deserve attention. For example, for emission enhancement, the energy from the excited molecules is first coupled to SPPs, which then radiatively scatter to far-field. To understand these two sequential processes completely, differentiating them one by one is necessary. Here, we decouple them and determine the coupling efficiency of molecules to SPPs by using a phenomenological rate equation model. We find the coupling efficiency, defined as the ratio of the coupling rate from molecules to SPPs to the direct Raman decay rate, can be expressed as the SERS intensity ratio and the SPP absorption and radiative decay rates, which all can be determined by polarization- and angle-dependent Raman and reflectivity spectroscopy. As a demonstration, the coupling efficiencies of 6-mercaptopurine to SPPs propagating in Γ-X direction on Ag nanohole array are measured for several Raman emission wavelengths.

Pioglitazone attenuates myocardial ischemia-reperfusion injury via up-regulation of ERK and COX-2.

Our previous study demonstrated that the peroxisome proliferator-activated receptor (PPAR) γ agonist, pioglitazone (PIO), may be cardioprotective against ischemia-reperfusion injury; however, modulation of p42/p44 extracellular signal-regulated kinases (ERK1/2) and cyclooxygenase (COX)-2 by PIO in the myocardium with respect to ischemia-reperfusion (I/R) is only partially understood. We determined if PIO reduces I/R-induced apoptosis in cardiomyocytes, and whether or not this protective effect is due to modulation of ERK1/2 and COX-2. Sixty male Sprague-Dawley rats were randomized and assigned to 1 of 6 groups: I/R; I/R + PIO (5 mg•kg(-1)•day(-1)); I/R + PIO (10 mg•kg(-1)•day(-1)); I/R + PIO (10 mg•kg(-1)•day(-1)) + the ERK1/2 inhibitor, PD98059; I/R + PIO ( 10 mg•kg(-1)•day(-1)) + GW9662;and I/R + PD98059. Rats underwent 30 min of myocardial ischemia and 120 min of reperfusion, and then hearts were harvested for analysis. RT-PCR and Western blotting were performed to detect expression of ERK1/2 and COX-2. The number of TUNEL-positive cardiomyocytes and NEC in the PIO groups (5 and 10 mg•kg(-1)•day(-1)) was much lower than the I/R group. The cardioprotective effect of PIO was abrogated by PD98059 and GW9662. Phosphorylation of ERK1/2 and COX-2 was increased in the PIO-treated group compared with the I/R group. GW9662 reversed the expression of ERK1/2 and COX- 2 phosphorylation induced by PIO. PD98059 reversed the expression of COX-2 induced by PIO. PIO was shown to be cardioprotective in an I/R injury model in rats via inhibition of cardiomyocyte apoptosis. PIO limited the infarct size in a PPAR-γ-dependent manner. These results show that PIO triggers the MAPK signaling pathway involving ERK1/2 using COX-2 as the downstream target.

Experimental use of a compact centrifugal pump and membrane oxygenator as a cardiopulmonary support system.

Compactness and high performance are the most important requirements for a cardiopulmonary support system. The Nikkiso (HPM-15) centrifugal pump is the smallest (priming volume; 25 ml, impeller diameter; 50 mm) in clinically available centrifugal pumps. The Kuraray Menox (AL-2000) membrane oxygenator, made of double-layer polyolefin hollow fiber, has a minimum priming volume (80 ml) and a low pressure loss (65 mm Hg at 2.0 L/min of blood flow) compared with other oxygenators. The aim of this study was to evaluate the performance of the most compact cardiopulmonary support system (total priming volume: 125 ml) in animal experiments. The cardiopulmonary bypass was constructed in a canine model with the Nikkiso pump and Menox oxygenator in comparison with a conventional cardiopulmonary support system. The partial cardiopulmonary bypass was performed for 4 h to evaluate the gas exchange ability, blood trauma, serum leakage, hemodynamics, and blood coagulative parameters. The postoperative plasma free hemoglobin level of the compact cardiopulmonary system was 29.5 +/- 10.21 mg/dl (mean +/- SD), which was lower than that of the conventional cardiopulmonary system, 48.75 +/- 27.39 mg/dl (mean +/- SD). This compact cardiopulmonary system provided the advantage in terms of reduction of the priming volume and less blood damage. These results suggested the possibility of miniaturization for the cardiopulmonary bypass support system in open-heart surgery in the near future.

Leukocyte-depleted reperfusion after long cardioplegic arrest attenuates ischemia-reperfusion injury of the coronary endothelium and myocardium in rabbit hearts.

OBJECTIVE: Cardiopulmonary bypass activates leukocytes, which should injure the coronary endothelium and myocardium during reperfusion especially after long cardioplegic arrest with long cardiopulmonary bypass time. The present study was designed to determine the protective efficacy of leukocyte-depleted reperfusion in blood-perfused parabiotic isolated rabbit hearts as a surgically relevant model with long cardioplegic arrest. METHODS: Each isolated rabbit heart, with a latex balloon inserted in the left ventricle, was parabiotically blood-perfused using a modified Langendorff column. The left ventricular developed pressure (DP), rate of pressure development (dP/dT), and coronary flow with a left ventricular end-diastolic pressure of 10 mmHg were measured before ischemia and after 15, 30, 45, and 60 min reperfusion after 4 h cardioplegic arrest kept at 20 degrees C (control, n=10). Leukocyte-depleted reperfusion was done in the test group (n=10). The endothelium of the coronary artery was observed by scanning electron microscopy (SEM) with percent injured area of endothelial cells measured to evaluate the extent of endothelial ischemia-reperfusion injury. RESULTS: The control hearts showed 53.3, 54.3, 48.4, and 39.0% recovery of DP compared to the pre-ischemia baseline data at 15, 30, 45, and 60 min after reperfusion began respectively. Leukocyte-depleted reperfusion enhanced the recovery of DP at 45 min (81.3%, P=0.0021) and 60 min (85.8%, P=0.0005) after reperfusion compared with that in the control group. The control hearts revealed 58.8%, 59.8%, 52.6%, and 43.4% recovery of dP/dT compared to the pre-ischemia baseline data at 15, 30, 45, and 60 min after reperfusion began, respectively. Leukocyte-depleted reperfusion also enhanced the recovery of dP/dT at 45 min (93.2%, P=0.0071) and 60 min (98.8%, P=0.0011) after reperfusion compared with that in the control group. There was also improvement of the recovery of coronary flow by leukocyte-depleted reperfusion (97.2%) compared with that in the control group (58.3%) after 60 min reperfusion (P=0.0121). Scanning electron microscopy showed that 69. 7% of coronary endothelial cells were morphologically injured in the control group. In contrast, leukocyte-depleted reperfusion prevented the extent of coronary endothelial damage with less injured area (0. 5%, P=0.0002). CONCLUSIONS: Leukocyte-depleted reperfusion improved functional recovery with reduced coronary endothelial injury after long cardioplegic arrest.

Ulinastatin attenuates reperfusion injury in the isolated blood-perfused rabbit heart.

BACKGROUND: Ventricular dysfunction after long cardioplegic arrest has been observed in cardiac operations. Urinary trypsin inhibitor, also called ulinastatin, may attenuate myocardial ischemia-reperfusion injury. The present study was designed to determine the protective efficacy of ulinastatin in blood-perfused parabiotic isolated rabbit hearts as a surgically relevant model with long (4-hour) cardioplegic arrest. METHODS: Each isolated rabbit heart, with a latex balloon inserted in the left ventricle, was parabiotically blood-perfused using a modified Langendorff column. The left ventricular developed pressure, rate of pressure development, and coronary flow with a left ventricular end-diastolic pressure of 10 mm Hg were measured before ischemia and 15, 30, 45, and 60 minutes after reperfusion began (control, n = 10). Ulinastatin (15,000 U/kg) was administered to the support animal just before reperfusion began (group U-1, n = 10) or at the beginning of the extracorporeal circulation and readministered before reperfusion (group U-2, n = 10). The endothelium of the coronary artery was observed by scanning electron microscopy to evaluate the extent of endothelial ischemia-reperfusion injury. RESULTS: Ulinastatin enhanced the recovery of developed pressure in both the U-1 (p<0.05) and U-2 (p < 0.01) groups compared with the control group. Although ulinastatin given just before reperfusion (group U-1) did not enhance the recovery of the rate of pressure development or the coronary flow compared with the control, earlier administration did improve the recovery of the rate of pressure development compared with the control (U-2, p<0.05), and there was improvement of the recovery of coronary flow after 60 minutes of reperfusion (U-2, p<0.05). Scanning electron microscopy showed that ulinastatin had ameliorated coronary endothelial damage. CONCLUSIONS: Ulinastatin improved functional recovery after long cardioplegic arrest and reduced coronary endothelial injury. Administration of ulinastatin at the beginning of cardiopulmonary bypass and just before reperfusion may be useful clinically in cases requiring prolonged aortic cross-clamping.

Does dilatation of the sinotubular junction cause aortic regurgitation?

BACKGROUND: Some patients develop aortic regurgitation (AR) in association with dilatation of the sinotubular junction (STJ), despite having normal aortic valve. However, the relationship between dilatation of the STJ and AR is unclear. METHODS: Canine hearts and aortas were isolated. A suture was placed in each commissure and in the sinus of Valsalva at the STJ. These interrupted sutures were drawn horizontally, and strain on the sutures was varied. The sites of the retracted sutures were changed to various positions, and the opening and closing of the aortic valve was observed endoscopically. A beating heart model was used to observe changes in aortic valve function during mechanical retraction of the commissures or sinuses. RESULTS: Opening area of the valve increased when strain on all sutures or commissures was increased. When strain was increased on the sinus alone, coaptation of the valve was not affected. CONCLUSION: We observed endoscopically that mechanical dilatation of the STJ causes AR. These findings suggest that the principal cause of AR associated with dilatation of the STJ is outward deviation of the commissure.

[Does dilatation of the sinotubular junction cause aortic regurgitation?: the use of the experimental model and preliminary result].

This study investigated the mechanism of aortic regurgitation caused by dilatation of the sinotubular junction. The canine model of dilatation of the sinotubular junction was used to observe coaptation of the aortic valve using direct imaging by endoscopy. Five adult mongrel dogs (body weight: 20-25 kg) were anesthetized and their hearts and thoracic aortas were extracted en bloc. Aortotomy was performed and an interrupted horizontal mattress suture was placed in each commissure and each sinus of Valsalva at the level of the sinotubular junction. The heart and thoracic aorta were fixed on a table and the interrupted sutures were drawn horizontally. As a result, the aorta of the junction level was dilated. Strain of the interrupted sutures were changed by weights of 20, 25, 50, 70 and 100 points (1 point = 3.5 g). The sites of the retracted sutures were the three commissures and three sinuses of Valsalva. With increased strain of the sutures, the opening of the aortic valve was exaggerated when drawing was done on either all sutures or the commissures. When drawing was done only on the three sinuses of Valsalva, coaptation of the aortic valve was uninterrupted. This study showed that dilatation of the sinotubular junction causes aortic regurgitation, which is mainly due to the outward deviation of the commissures.

Veno-right ventricular extracorporeal membrane oxygenation for thoracic surgery: an experimental study in dogs.

BACKGROUND: Although the indications for extracorporeal membrane oxygenation (ECMO) have been extended, ECMO has yet to be used as a respiratory support system during thoracic surgery. The purpose of this experimental study was to investigate whether veno-right ventricular (veno-RV) ECMO can be used for thoracic surgery without mechanical ventilation. METHODS: Acute experimental study: Veno-RV ECMO as total lung support was maintained for 60 min without mechanical ventilation in six dogs. A venous drainage cannula was inserted in the superior cavoatrial junction through the right femoral vein and a venous return cannula was inserted in the right ventricle through the right jugular vein. The veno-RV ECMO system comprised a centrifugal pump and membrane oxygenator. Survival model: After veno-RV ECMO had been established in three dogs, a two-ring thoracic tracheal segment was resected and the tracheal ends were anastomosed by video-assisted thoracic surgery without ventilation. RESULTS: In the acute study, when the veno-RV ECMO flow was maintained at 100 mL/kg/min, all six dogs remained hemodynamically stable and the arterial oxygen saturation was maintained at more than 98%, despite total lung collapse. In the survival study, all three dogs made an uneventful postoperative recovery. CONCLUSION: Video-assisted tracheal surgery can be performed without conventional respiratory support. Veno-RV ECMO as total lung support may become an alternative respiratory management device for thoracic surgery.

Veno-right ventricle bypass as a lung support system during pulmonary surgery without ventilation.

A special lung support technique is required during carinal or tracheal surgery Veno-venous extracorporeal membrane oxygenation (ECMO) has become an accepted technique for temporary lung support. Therefore, the purpose of our experiments was to evaluate the effect of veno-venous ECMO (veno-right ventricle bypass) without ventilatory support. In five mongrel dogs, two venous drainage cannula were inserted into the superior vena cava through the right jugular vein and the inferior vena cava through the right femoral vein. In addition, a venous return cannula was inserted into the right ventricle (RV) through the right jugular vein. The veno-right ventricle (veno-RV) bypass system was composed of a centrifugal pump and membrane oxygenator; pump flow was maintained at 88 +/- 14 ml/kg/min. Excellent hemodynamics and good oxygenation were obtained. On the basis of these results, we conclude that veno-RV bypass may be used as lung support during pulmonary surgery even though the native lung is not ventilated during the veno-RV bypass procedure.