A pitfall in the xanthine oxidase hypothesis.
Explore the source record for details and available documents.
Animals↗
Biomedical subjects
K Irita
Publications and source records attributed to K Irita.
Contribution of arterial redox potential measurement to the care of critically ill patients.
175 arterial and 122 urinary samples from 20 patients admitted in ICU for organ system failure (OSF) were analysed. Besides arterial blood gases and lactate, electrolyte concentrations, pH, rH2 and specific resistance (R) in blood and urine were measured. Redox potential (E) and base excess were calculated from these data. Patients were defined as having MOSF if their organ systems met failure criteria during their ICU stay. Data were classified with corresponding number of OSF developed in the patients when samples were obtained. Acid-base balance or base excess alone could not be used to predict the severity of illness as assessed by increasing number of organ system failures. Significant elevations in blood lactate concentrations were observed only in patients with four, five or six OSF. A lack of correlation between blood lactate and severity of OSF indicates that blood lactate is not valid as a guide to ultimate outcome of the patients. Arterial redox potentials progressively decreased with increasing number of OSF, therefore, it can be stated that the serial measurements of arterial redox potential are useful in assessing the patient's status or predicting their ultimate outcome.
Journal Article↗
The bioelectronic factors of human body fluids and intravenous replacement solutions.
In this paper the analytical method of the pH, rH2 and specific resistance of body fluids with B.E.-VINCENT Unit was described. From the values of the pH, rH2 and specific resistance, other three bioelectronic factors, the redox potential, milliampere and micro-watts, were calculated. With this technique the bioelectronic factors of arterial and venous blood and urine obtained from 20 young healthy adults were examined. Those of arterial and venous blood showed almost identical values. The urinary values of the pH, milliampere and microwatts varied as compared to those of blood. The bioelectronic factors of the various intravenous replacement solutions and blood components were considerably different from those of blood. It is considered that the bioelectronic factors of patient's blood should be checked repeatedly and maintained in an appropriate state when massive fluid therapy is required.
Journal Article↗
Calcium channel antagonist induced inhibition of superoxide production in human neutrophils. Mechanisms independent of antagonizing calcium influx.
Three calcium channel antagonists, verapamil, diltiazem and nisoldipine, inhibited superoxide production in human neutrophils that were stimulated by phorbol 12-myristate 13-acetate (PMA) in a buffered saline lacking calcium. Concentrations of these drugs giving 50% control activity (IC50) were 0.3, 0.45 and 0.01 mM respectively. This inhibition was also observed in the presence of ethylene glycol bis (beta-aminoethyl ether)-N,N'-tetraacetic acid (EGTA) and was not reversed by the addition of calcium. This suggests that calcium channel antagonists inhibited superoxide production independently of extracellular calcium. These calcium channel antagonists inhibited the mobilization of membrane-associated calcium, and protein phosphorylation probably catalyzed by C-kinase, both of which are thought to be involved in the signal transmission for the induction of superoxide production. Calcium channel antagonists also inhibited NADPH oxidase, responsible for superoxide production, with IC50 = 0.5, 3 and more than 0.08 mM, respectively, for verapamil, diltiazem and nisoldipine. The results indicate that calcium channel antagonists inhibit superoxide production by affecting not only the catalytic activity by also the activation of NADPH oxidase. Inhibition of superoxide production by calcium channel antagonists suggests that these antagonists do not affect cell functions merely by affecting calcium influx.
Calcium↗
Protein phosphorylation of neutrophils from normal children and patients with chronic granulomatous disease.
The phosphorylation and dephosphorylation of proteins in neutrophils from normal children and patients with chronic granulomatous disease (CGD) were studied with two-dimensional gel electrophoresis and autoradiography, followed by densitometric scanning. In normal neutrophils the radioactivities of 11 spots among approximately 50 radioactive spots were changed by stimulation with phorbol 12-myristate 13-acetate (PMA) and 6 of the 11 spots were also changed by stimulation with N-formyl-methionyl-leucyl-phenylalanine (FMLP) and NaF. The phosphorylation of only two spots (Mr = 48 000 and 62 000) was inhibited by 2-deoxyglucose and N-(6-aminohexyl)-5-chloro-1-naphthalene sulphonamide (W-7), which inhibits superoxide production, while it was not affected by dibutyryl cAMP, KCN and ethyleneglycol-bis-(beta-aminoethylether)-N,N'-tetraacetic acid (EGTA), which do not affect superoxide production. The observation indicates that the Mr = 48 000 and 62 000 proteins may be involved in the activation process of superoxide production. When the neutrophils of four male and two female CGD patients were examined, the changes in 11 spots on stimulation were similar to those of normal children, indicating that the (de)phosphorylation of the proteins which seems to be involved in the activation process is not affected in CGD neutrophils.
Autoradiography↗
Cinchocaine and amethocaine inhibit activation and activity of superoxide production in human neutrophils.
Local anaesthetics, cinchocaine and amethocaine, inhibited superoxide production in human neutrophils stimulated by phorbol ester, with IC50 (concentration of a drug giving 50% activity of control) values of 0.2 and 0.6 mmol litre-1, respectively. These anaesthetics inhibited protein (de)phosphorylation and mobilization of membrane-associated calcium, both of which are probable signal transmission mechanisms for the induction of superoxide production. Local anaesthetics also inhibited NADPH oxidase, responsible for superoxide production, with IC50 = 0.3 and 0.9 mmol litre-1, respectively. The results indicate that cinchocaine and amethocaine inhibit superoxide production in human neutrophils by affecting not only the catalytic activity, but also the activation, of NADPH oxidase.
Blood Proteins↗
Protein phosphorylation in intact pig leukocytes.
The phosphorylation of proteins in intact pig polymorphonuclear leukocytes loaded with H3(32)PO4 was investigated by two-dimensional gel electrophoresis and subsequent autoradiography. The incorporation of 32P into at least 17 proteins began to increase and into one to decrease, relative to resting cells, upon exposure of the cells to phorbol 12-myristate 13-acetate. These changes in the autoradiographic patterns were accompanied by changes in the protein patterns obtained by staining with Coomassie brilliant blue, including the appearance, the acidic shift and the increase or decrease of the intensity of the spots. Among these proteins, Mr = 64 000, 31 000, 22 000, 21 000, 18 000 and 13 000 proteins were correlated well with the superoxide anion production of the cells in respect to the time-courses and the dose-responses. By taking the effects of EGTA into consideration, the phosphorylation of Mr 64 000 and 21 000 proteins, of which the latter was identified as the light chain of myosin, seemed to be involved in the signal-transmission mechanism of the induction of the NADPH oxidase responsible for the 'respiratory burst'. These two proteins were also phosphorylated in the cells stimulated by NaF or oil droplets opsonized with IgG.
Animals↗
Diacylglycerol, 1-oleoyl-2-acetyl-glycerol, stimulates superoxide-generation from human neutrophils.
1-Oleoyl-2-acetyl-glycerol which activates Ca2+-activated phospholipid-dependent protein kinase, induced the superoxide-production of human neutrophils, while other diacylglycerols did not. The induction was independent of extracellular calcium and did not accompany the increase of the intracellular free calcium. The superoxide-release by the diacylglycerol was inhibited by retinal, the inhibitor of the protein kinase. The diacylglycerol stimulated the phosphorylation of at least 4 proteins in intact neutrophils, the phosphorylation of which was stimulated by phorbol 12-myristate 13-acetate, the activator of the protein kinase. These observations indicate the possible involvement of the kinase in the induction process.
Diglycerides↗
Phosphorylation of myosin light chain in intact pig leukocytes stimulated by phorbol 12-myristate 13-acetate.
Phosphorylation of myosin light chain was investigated in intact pig polymorphonuclear leukocytes. The labeling of the myosin light chain (Mr = 21000) was increased by exposure of the cells to phorbol 12-myristate 13-acetate. Two-dimensional gel electrophoresis revealed three forms of Mr = 21000 light chain, of which two were phosphorylated. The phosphorylation of the myosin light chain was inhibited by neither N-(6-aminohexyl)-5-chloro-1-naphthalene sufonamide nor trifluoperazine, suggesting that calmodulin is not involved in the phosphorylation.
Animals↗
Superoxide formation by neutrophils during phagocytosis.
Explore the source record for details and available documents.
Animals↗
Arterial to end-tidal CO2 gradient as an adjunct to unmasking silent pulmonary embolism.
Explore the source record for details and available documents.
Anesthesia↗
Whole body oxygen consumption during extracorporeal hepatic resection: usefulness of continuous monitoring of mixed venous oxygen saturation.
Whole body oxygen consumption was measured using a thermodilution fibreoptic catheter in two patients undergoing extracorporeal hepatic resection. Each patient had virtually normal liver function before the operation. Anaesthesia was induced and maintained in a standard fashion and a venovenous bypass instituted. The anhepatic periods were 302 and 157 min. Upon removal of the liver, the oxygen consumption decreased by about 40% (50 mL/min), while the mixed venous oxygen saturation increased by about 15%. Following re-implantation, the oxygen consumption recovered and increased transiently above control values, while the mixed venous oxygen saturation changed in a reciprocal way. Monitoring whole body oxygen consumption instead of hepatic oxygen consumption seemed helpful in estimating restoration of blood flow and functions in the liver after reperfusion. It was also suggested that changes in oxygen consumption as well as those in cardiac output and haemoglobin concentration could be predicted easily by continuous monitoring of mixed venous oxygen saturation during the peri-anhepatic period.
Cardiac Output↗
The effects of dichloroacetate on liver damage and circulating fuels in rats exposed to carbon tetrachloride.
It has been known that carbon tetrachloride-induced liver damage in starved rats is ameliorated simply by restoration of feeding. An analogue of dichloroacetate has been reported to ameliorate carbon tetrachloride-induced liver damage, and dichloroacetate has been shown to have a variety of effects on fuel metabolism. We investigated simultaneously the effects of dichloroacetate on liver damage and on circulating fuels in rats exposed to carbon tetrachloride. The effects of carbon tetrachloride varied with the rat's condition. In starved rats, the liver damage was more severe, and serum ketone body concentration decreased. In non-starved rats, the liver damage was not as severe and the serum ketone body concentration increased. The administration of dichloroacetate ameliorated liver damage both in starved and in non-starved rats given carbon tetrachloride: the administration of dichloroacetate protected from the liver damage particularly in starved rats. There were associated changes in the concentrations of circulating fuels. When the pyruvate-lowering effect of dichloroacetate was diminished in carbon tetrachloride-injected, starved rats, the alanine aminotransferase-lowering effect of dichloroacetate was also diminished. We propose that dichloroacetate's effect on fuel metabolism may produce a hepato-protective effect.
Alanine Transaminase↗