Effects of increased surface coverage of polyvinylpyrrolidone over a polysulfone hemofilter membrane on permeability and cell adhesion during continuous hemofiltration.

The purpose of the present study was to evaluate the adhesiveness of blood cells and the solute removal performance change of modified polysulfone membranes which have increased polyvinylpyrrolidone (PVP) coverage over their surface. Continuous hemofiltration (CHF) experiments for 24 h were carried out using an ex vivo hemofilter evaluation system to compare a modified polysulfone hemofilter (SHG) with the conventional polysulfone hemofilter (SH). The 25 and 50 % cutoff values of the sieving coefficient of dextran after CHF and the protein concentration in the filtrate was higher in SHG, indicating that less fouling occurred in the SHG membrane. Adhesion of blood cells after 24 h of CHF was significantly higher in the case of SH than in the case of SHG. Blood cell adhesion and membrane fouling were reduced with the use of a polysulfone membrane modified with increased PVP coverage over the surface.

Breathing nitric oxide plus hydrogen gas reduces ischemia-reperfusion injury and nitrotyrosine production in murine heart.

Inhaled nitric oxide (NO) has been reported to decrease the infarct size in cardiac ischemia-reperfusion (I/R) injury. However, reactive nitrogen species (RNS) produced by NO cause myocardial dysfunction and injury. Because H2 is reported to eliminate peroxynitrite, it was expected to reduce the adverse effects of NO. In mice, left anterior descending coronary artery ligation for 60 min followed by reperfusion was performed with inhaled NO [80 parts per million (ppm)], H2 (2%), or NO + H2, starting 5 min before reperfusion for 35 min. After 24 h, left ventricular function, infarct size, and area at risk (AAR) were assessed. Oxidative stress associated with reactive oxygen species (ROS) was evaluated by staining for 8-hydroxy-2'-deoxyguanosine and 4-hydroxy-2-nonenal, that associated with RNS by staining for nitrotyrosine, and neutrophil infiltration by staining for granulocyte receptor-1. The infarct size/AAR decreased with breathing NO or H2 alone. NO inhalation plus H2 reduced the infarct size/AAR, with significant interaction between the two, reducing ROS and neutrophil infiltration, and improved the cardiac function to normal levels. Although nitrotyrosine staining was prominent after NO inhalation alone, it was eliminated after breathing a mixture of H2 with NO. Preconditioning with NO significantly reduced the infarct size/AAR, but not preconditioning with H2. In conclusion, breathing NO + H2 during I/R reduced the infarct size and maintained cardiac function, and reduced the generation of myocardial nitrotyrosine associated with NO inhalation. Administration of NO + H2 gases for inhalation may be useful for planned coronary interventions or for the treatment of I/R injury.

Activation of platelets upon contact with a vitamin E-coated/non-coated surface.

The purpose of this study was to determine the effects of a vitamin E-coated surface on platelet activation, focusing on the interactions among the vitamin E-coated surface, platelets and leukocytes. Platelet-rich plasma (PRP) or PRP containing leukocytes (LPRP) was used. No difference was observed in platelet activation between PRP and LPRP for a vitamin E-coated membrane, meaning that platelet activation triggered by leukocytes was suppressed in plasma coming in contact with a vitamin E-coated membrane, while the membrane itself directly induced platelet activation. The antioxidant capacity of the vitamin E-coated membrane in contact with PRP or LPRP was partially reduced, but sufficient residual capacity remained. The in vitro experiments using an oxidized vitamin E-coated surface revealed that P-selectin expression and superoxide anion production in the platelets and platelet adhesion were induced by contact with the oxidized vitamin E-coated surface. We conclude that contact with a vitamin E-coated surface reduces platelet activation mediated by superoxide anions, probably by reducing superoxide anions, but during the process of the reduction, the vitamin E-coated surface itself becomes oxidized, which again causes platelet activation. The beneficial effects of a vitamin E-coated dialyzer in respect of platelet activation were counteracted by the formation of oxidized vitamin E.

X-ray radiation causes electromagnetic interference in implantable cardiac pacemakers.

BACKGROUND: X-rays are not thought to cause electromagnetic interference (EMI) in implantable cardiac pacemakers. However, x-ray radiation during computed tomography (CT) scanning has been reported to cause EMI in some implantable cardiac pacemakers. The objectives of this study were to identify the location within the pacemakers where x-ray radiation causes EMI and to investigate the association of EMI with the x-ray radiation conditions. METHODS: We verified the location where x-ray radiation caused EMI using a CT scanner and conventional radiographic x-ray equipment. An inhibition test and an asynchronous test were performed using five types of implantable cardiac pacemakers. RESULTS: X-ray radiation inhibited the pacing pulses of four types of implantable cardiac pacemakers when the body of each implantable cardiac pacemaker, containing a complementary metal-oxide semiconductor (CMOS), was scanned using a CT scanner. We confirmed that x-ray-induced EMI depends on the x-ray radiation conditions, that is, the tube voltage, tube current, x-ray dose, and direction of x-ray radiation, as well as the sensing thresholds of the implantable cardiac pacemakers. CONCLUSIONS: X-ray radiation caused EMI in some implantable cardiac pacemakers, probably because the CMOS component was irradiated. The occurrence of EMI depended on the pacemaker model, sensing threshold of the pacemaker, and x-ray radiation conditions.

Macrophages that survive hyperoxia exposure have higher superoxide dismutase activities in their mitochondria.

Prolonged exposure to hyperoxia, which is routinely used in patients with severe respiratory failure, leads to the generation of excessive reactive oxygen species, resulting in lung injury. In the present study, we focused on macrophages and their survival, superoxide dismutase (SOD) activity in mitochondria (Mn-SOD activity), and mitochondrial DNA (mtDNA) mutation after exposure to hyperoxia. Macrophages were cultured under two different conditions: normoxia and intermittent hyperoxia. The number of cells exposed to intermittent hyperoxia for 3 weeks significantly decreased, compared with the number of cells exposed to normoxia. The Mn-SOD activity of the cells that survived intermittent hyperoxia exposure was significantly higher than that of the cells exposed to normoxia. Direct sequencing and a PCR-RFLP assay did not provide any evidence of mutation in the cells that survived intermittent hyperoxia exposure. In conclusion, an increase in the antioxidative activity of mitochondria is important for the survival of macrophages exposed to hyperoxia, and the increased activity level possibly enhances protective effects against mtDNA mutations in surviving cells.

Synchronization between cardiac and respiratory rhythms in healthy subjects and patients.

Synchronization between cardiac and respiratory rhythms may be important for oxygen transport to tissues. The aim of this study was to investigate the synchronization between cardiac and respiratory rhythms. We evaluated the rhythms in 12 healthy males and 24 patients. The incidence rates of heart beats were obtained in each time interval relative to the initiation time point of inspiration. A simple index of timing variability of heart beats was defined. When the variability is large, the link between cardiac and respiratory rhythms was considered to be strong. The variability value of patients with disorder in the autonomic nervous system was larger than that of healthy subjects (p < 0.05). The variability of patients on controlled ventilation was lower than that of healthy subjects (p < 0.01), whereas the value on cardiac pacemaker did not differ from healthy subjects. In conclusion, the synchronization between cardiac and respiratory rhythms was confirmed, and it is suggested that the synchronization is enhanced when feed-back signals from respiratory movement to respiratory center were decreased.

Study of light transmission through gauze pad effected by blood or liquids to detect needle dislodgement.

OBJECTIVE: Serious accidents during hemodialysis such as a large amount of blood loss are often caused by venous needle dislodgement. To develop a bleeding sensor based on a photo sensor for monitoring the needle sites, we studied effects of liquids and porcine blood on light transmission through a thin gauze pad with a basic photo sensor. METHODS: The photo sensor consisted of an ordinary electrical circuit, a light emitting diode (LED, lambda max = 645 nm), a photo diode (PD), and a thin gauze pad placed between the LED and PD that were tightly attached to the edges of a plastic clip. The light transmitted through the gauze pad, soaked with liquids or porcine blood dropped on it, was measured with a digital voltmeter. The liquids were reverse osmosis water, physiological saline, glucose in water at 5, 10, 20, 40 and 50%, porcine plasma, and porcine blood (Hct 40, 30 and 20%). RESULTS: The liquids on a tight-weave gauze pad, significantly increased the voltage (light transmission) from 0.412 +/- 0.003 V (SD) to 0.794 +/- 0.025 V (minimum, by reverse osmosis water) and to 0.945 +/- 0.011 V (maximum, by 50% glucose). The porcine blood significantly decreased the voltage from 0.412 to 0.195 +/- 0.030 V in Hct 40%, to 0.334 +/- 0.035 in Hct 30%, to 0.397 +/- 0.007 V in Hct 20%. The higher the concentration of glucose, the more the light transmission increased. The higher concentration of Hct, the more the light transmission decreased. Similar results were also shown for the loose-weave pad. CONCLUSIONS: Using two types of gauze pads, we confirmed that liquids significantly increased light transmission through gauze pad, but porcine blood decreased light transmission. This opposite response can be used to distinguish liquids from blood on a gauze pad.

The role of nitric oxide in reducing deformability of Lewis lung tumor cell stimulated by inflammatory cytokines.

Highly metastatic cells, especially in the lungs, are known to be resistant to nitric oxide (NO)-mediated cytotoxicity, compared with poorly or non-metastatic cells. However, the precise mechanisms connecting NO and metastasis remain to be determined. To clarify the role of NO in the characteristic changes in NO-resistant cells in response to inflammatory cytokines, we used Lewis lung tumor (LLT) cells, which are known to be highly metastatic NO-resistant cells, and determined the changes in cell deformability and the gene expression profile after the cells were stimulated using cytokine mixture or an NO donor. Both exogenous NO and endogenous NO via inducible NO synthase produced by cytokines decreased cell deformability by enhancing actin polymerization. The expression of several genes associated with actin polymerization was changed so as to increase actin filaments in the cells by enhancing actin polymerization and by suppressing actin depolymerization, actin filament severing, and barbed-end actin filament capping. In conclusion, inflammatory cytokine stimulation reduces deformability of LLT cells and enhances actin polymerization which is mainly controlled by the same genes induced by NO.

Bench study of auto-CPAP devices using a collapsible upper airway model with upstream resistance.

The aim of this study was to investigate the response of auto-CPAP devices to respiratory events (apnea, hypopnea, flow-limitation and snoring) on the same condition using a physiological upper airway model. The hypothesis of this study is that collapsibility of the flow-limiting collapsible segment of the airway is influenced by the upstream airway resistance. Five auto-CPAP devices, AutoSet T, AutoSet Spirit, Goodnight 420E, PV10i and REMstar Auto were evaluated. Apnea: all the devices increased the auto-CPAP level, while AutoSet T and AutoSet Spirit did not respond to apnea for 30s. Hypopnea: all the devices except the AutoSet T and Goodnight 420E increased pressure. Flow-limitation: all the devices except the PV10i and REMstar Auto increased pressure. Snoring: the snoring sounds disappeared when REMstar Auto and PV10i were used, and the Goodnight 420E lowered the level of snoring. In conclusion, the response of auto-CPAP devices to respiratory events differed. Collapsible upper airway model with upstream resistance is useful for the first-step assessment of auto-CPAP devices.

[Verification of irradiation conditions of X-rays that influence implantable cardiac pacemakers].

Originally, it was thought that X-rays did not influence implantable cardiac pacemakers. In general, radiological technologists did not take proper care of these devises at the time of X-Ray examinations. However, 11 cases in which pacemakers malfunctioned (for example partial electrical reset) during CT examinations have been reported in recent years. At the time, we tended to attribute such problems to the peculiarities of multi-detector CT (MDCT). However, on logical grounds this explanation seemed weak. To better explain the problem, we attempted various tests in which pacemakers were exposed to CT and X-ray photography equipment. We analyzed some ECG results to clarify the matter and took measurements to examine these problems.

Hypoxia enhances the induction of human amniotic mesenchymal side population cells into vascular endothelial lineage.

Human amniotic mesenchymal side population (hAM-SP) cells have pluripotency and weak immunogenicity, and have promising roles in the field GAPDH of regenerative medicine. The aim of the present study was to determine whether hypoxic conditions induce the differentiation of hAM-SP cells into the vascular endothelial lineage. Mesenchymal cells were isolated from enzyme-treated amniotic membranes and stained with Hoechst 33342. The hAM-SP cells were negatively sorted by FACS and cultured in induction medium containing vascular endothelial growth factor (VEGF) under normoxic (20% O2) or hypoxic (1% O2) conditions for 1 or 2 weeks. The expression of endothelial markers such as kinase domain region (KDR), fms-like tyrosine kinase (Flt)-1, von Willebrand factor (vWF), vascular endothelial (VE)-cadherin and human vascular cell adhesion molecule (VCAM) at the gene and protein level was evaluated by real-time PCR and fluorescent immunostaining, respectively. The gene expression of KDR, Flt-1, VE-cadherin and vWF peaked after 2 weeks of culture. The protein expression of KDR and VE-cadherin was also enhanced after 2 weeks of culture under hypoxic conditions. To confirm the involvement of hypoxia-inducible factor (HIF) in the induction under hypoxic conditions, the expression of genes which are known to be upregulated by HIF was analyzed by DNA microarray. The expression of these genes increased under hypoxic conditions. hAM-SP cells cultured under hypoxic conditions differentiated into the vascular endothelial lineage, probably due to upregulation of the gene expression associated with angiogenesis through activation of the HIF system.