The role of neutrophil and its chlorinated oxidant were investigated in Helicobacter pylori-induced gastric mucosal injury in vitro. Luminol-dependent chemiluminescence (ChL) was used to detect neutrophil-derived oxidants. ChL activity was significantly elevated when neutrophils were incubated in H. pylori, indicating that H. pylori actually elicits oxidative burst of neutrophils. To assess whether H. pylori-activated neutrophils exert the cytotoxicity for gastric mucosal cells, rabbit gastric mucosal cell was monolayered in culture wells and labeled with a fluorescence dye, 2',7'-bis(2-carboxyethyl)-5(6)carboxy-fluorescein, which is retained in the intracellular space as long as the cell membrane is intact. Labeled cells were coincubated with neutrophils and H. pylori. We inferred from the cytotoxicity index (specific %cytotoxicity), which was calculated from fluorometrical measurements of supernatant and lysate, that the mucosal cells were significantly damaged by H. pylori-activated neutrophils. This injury was largely attenuated by eliminating urea from the incubation mixture or by acetohydroxamic acid, a potent urease inhibitor. Additionally, the scavengers of neutrophil-derived oxidants, including taurine, methionine, and catalase, also attenuated this injury. Cultured mucosal cells that were exposed to the solution containing monochloramine (an oxidant yielded by reaction of hypochlorous acid and ammonia) were highly damaged compared with cells exposed to hypochlorous acid or hydrogen peroxide at physiological concentrations. These data suggest that H. pylori-activated neutrophils promote gastric mucosal cell injury and that monochloramine plays a unique and important role in this process.

The present experiments were carried out to investigate the usefulness of measuring peripheral tissue metabolism for the clinical assessment of shock. Male Wistar/ST rats (8 weeks-old) were used. All rats were placed in a supine position while anesthetized. A tube for measuring arterial pressure and collecting blood samples was cannulated into the femoral artery. For microdialysis, the introducer was inserted into the subcutaneous tissue in the abdominal wall. Blood was exsanguinated to maintain the mean arterial pressure at 40 +/- 5 mmHg. Mean arterial pressure, arterial blood gas and serum lactate levels were measured. Microdialysis was performed to quantify the levels of lactate and pyruvate in the subcutaneous tissue. Six rats died due to hemorrhagic shock by 350 min (Group D) while six rats had survived for the 350 min period after exsanguination (Group A). These data was obtained at intervals of 50 min after exsanguination up to a period of 250 min and compared between Groups A and D. In Group A, serum lactate levels did not increase throughout the entire period of observation. Serum lactate levels in Group D transiently increased, but did not show a dramatic increase during the blood pressure maintenance period. In particular, serum lactate levels increased again after a period of more than 150 min following exsanguination. Lactate levels in the subcutaneous tissue gradually increased and were significantly higher in Group D than that in Group A after 150 min. The L/P ratio in Group A remained fairly constant during the period of observation. In contrast, the L/P ratio in Group D increased gradually, and was significantly higher than that in Group A after 100 min. It was concluded that the continuous increase in the L/P ratio in the subcutaneous tissue in Group D was indicative of tissue circulatory failure and of an abnormality in tissue oxygen metabolism prior to the detection of the collapse of compensatory mechanisms appearing in the vital signs. These findings suggest that measuring the L/P ratio is useful for the clinical assessment and monitoring of shock.

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Reynolds-averaged Navier-Stokes simulations (RANS) of flows around a Clark-Y airfoil with uniform blowing (UB) and uniform suction (US) are performed aiming at improvement of the airfoil performance. First, the control effect in the case with single UB or US applied on the airfoil surface is investigated at the various control locations. The magnitude of UB/US is 0.14% of the free-stream velocity, and the control region is set at four different locations on the upper and lower surfaces. The Reynolds number based on the chord length and the angle of attack are 1.5 × 10 6 and 0 • , respectively. It is found that the friction drag is decreased/increased by single UB/US control. It is also found that UB on the lower surface or US on the upper surface improves the lift-to-drag ratio, while UB on the upper surface or US on the lower surface worsens it. In the combined control of UB and US having the equal flow rate, the magnitude of blowing and suction is set at 0.14% or 0.26% of the free-stream velocity. The locations of blowing/suction and flow conditions are the same as those in the cases with either UB or US only. The simulation result suggests that the lift-to-drag ratio is improved by the combined control of UB on the lower surface and US on the upper surface. In particular, the lift-to-drag ratio is most improved by a combination of UB on the lower rear surface and US on the upper rear surface. In contrast, a combined control of UB on the upper front surface and US on the lower rear surface is identified as the most effective case for the friction drag reduction only.

Purpose: Tissue dysoxia is thought to be a fundamental cause of the organ failure that occurs as a result of shock. Plasma lactate has been frequently measured as an indicator of the state of systemic tissue metabolism. On the other hand, tissue lactate levels can directly indicate a disorder in the state of cytological tissue metabolism. The continuous monitoring of lactate levels in subcutaneous tissue will reflect the state of tissue dysoxia more precisely than levels of lactate in the plasma lactate. We have investigated the differences in the levels of plasma and tissue lactate using a microdialysis (MD) technique in an animal septic shock model. Method: Male 8-week-old Wistar/ST rats were used. We prepared an animal model by injection of lipopolysaccharide (LPS) into the abdominal cavity. LPS was given to 9 animals in the experimental group while physiological saline was given to 6 animals in the control group. A MD probe was used to quantify the lactate levels in the subcutaneous tissue. The mean arterial pressure, blood gas content and lactate levels were measured every 50 min up to 400 min after injection and compared between both groups. Result: The MAP of both groups showed similar changes after injection. Plasma lactate levels in the LPS group showed a significant increase after 100 min and reached a plateau from 150 min to 250 min. Subcutaneous lactate in the LPS group showed a significant increase after 150 min. Subcutaneous pyruvate in the LPS group showed a significant increase after 100 min. The lactate/pyruvate (L/P) ratio in the subcutaneous tissue showed a sustained increase from 300 min in the LPS group. Conclusion: Monitoring plasma lactate levels is useful for the early assessment of anaerobic metabolism before hypotension. Plasma lactate levels did not increase during some periods. This phenomenon was due to the balance between production and utilization. However, tissue lactate showed a chronological increase. These results suggest that the measurement of tissue lactate levels is reliable for assessing local energy metabolic disturbances. Under conditions of septic shock, an increase in lactate levels was found to be a sensitive marker of tissue metabolism disorder.