RESUMO
An experimental study of two-phase flow pressure drop using R-134a is conducted on three types of different surface wettability microchannels with superhydrophilic (contact angle of 0°), hydrophilic (contact angle of 43°) and common (contact angle of 70°, unmodified) surfaces, all with a hydraulic diameter of 0.805 mm. Experiments were conducted using a mass flux of 713-1629 kg/m2s and a heat flux of 7.0-35.1 kW/m2. Firstly, the bubble behavior during the two-phase boiling process in the superhydrophilic and common surface microchannel is studied. Through a large number of flow pattern diagrams under different working conditions, it is found that the bubble behavior shows different degrees of order in microchannels with different surface wettability. The experimental results show that the hydrophilic surface modification of microchannel is an effective method to enhance heat transfer and reduce friction pressure drop. Through the data analysis of friction pressure drop and C parameter, it is found that the three most important parameters affecting the two-phase friction pressure drop are mass flux, vapor quality, and surface wettability. Based on flow patterns and pressure drop characteristics obtained from the experiments, a new parameter, named flow order degree, is proposed to account for the overall effects of mass flux, vapor quality, and surface wettability on two-phase frictional pressure drop in microchannels, and a newly developed correlation based on the separated flow model is presented. In the superhydrophilic microchannel, the mean absolute error of the new correlation is 19.8%, which is considerably less than the error of the previous models.
RESUMO
OBJECTIVE: To evaluate the expression of vascular cell adhesion molecules (VCAM-1) and eotaxin and their transcription factors NF-kappa B and AP-1 in bronchi and bronchioles (with surrounded lung tissue), and to investigate the mechanisms for eosinophil chemotaxis to the lungs in a guinea pig model of asthma. METHODS: (1) The guinea pig model of asthma was established by the ovalbumin challenge method. (2) The animal models were divided into six groups: control, asthma day 1, asthma day 4, asthma day 14, intraperitoneal dexamethasone, and budesonide inhalation groups. (3) The protein expressions of VCAM-1, eotaxin, NF-kappa B and AP-1 in segmental bronchi and in bronchioles and lung tissue were measured by immunohistochemical techniques. (4) The mRNA expressions of VCAM-1 and eotaxin in lung tissue homogenates were determined by RT-PCR. (5) The DNA binding activities of NF-kappa B and AP-1 were measured by electrophoretic mobility shift assay (EMSA). RESULTS: (1) In all the asthmatic groups, the protein levels of VCAM-1, eotaxin, NF-kappa B and AP-1, expressed both in central and peripheral airways (26.3 +/- 3.2, 89.0 +/- 8.6, 179 +/- 7 and 76 +/- 6), were significantly elevated compared to those in the control group (11.2 +/- 3.7, 5.0 +/- 4.0, 36 +/- 3 and 27 +/- 5). (2) The mRNA expression levels of VCAM-1 and eotaxin in lung tissue homogenates were significantly higher in the asthmatic groups (2.46 +/- 0.38 and 1.080 +/- 0.080) than those in the control group (1.05 +/- 0.11 and 0.080 +/- 0.020). (3) The DNA binding activities of NF-kappa B and AP-1 were significantly increased in the asthmatic groups (256 +/- 10 and 78 +/- 14), than those in the control group (67 +/- 13 and 12 +/- 3). (4) All these parameters in both glucocorticoid treated groups were significantly decreased compared to those in the asthma day 14 group, and similar to those in the control group. CONCLUSIONS: VCAM-1 and eotaxin actively participated in the process of eosinophilic inflammation. NF-kappa B and AP-1 may play important roles in the regulation of VCAM-1 and eotaxin. The up- regulation of these inflammatory mediators existed not only in central airways, but also in small airways and lung tissue, indicating that asthma in this model is a disease of whole respiratory system. Glucocorticoids, either by systemic use or inhalation, demonstrated antiinflammatory effects by inhibiting the expressions and activities of NF-kappa B and AP-1 and by down-regulation of VCAM-1 and eotaxin.
