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Biomedical subjects

K Niizeki

Publications and source records attributed to K Niizeki.

At least 19 recordsLinked to original sources
PubMed1992

Behavior of cardiac output during progressive exercise tests: a preliminary report.

The behavior of cardiac output (Q) during progressive incremental exercise tests was studied in young healthy men. Q approached a plateau and leveled off at almost the same work rate at which oxygen uptake (VO2) attained its maxima, while heart rate (HR) still continued to rise. This suggests that the limiting factor for maximal aerobic capacity in healthy subjects is Q. The rate of increase in Q and HR accelerated from a work rate which is close to the ventilatory anaerobic threshold (AT). The prime cause of the progressive augmentation in cardiac activity is probably an accelerated release of plasma catecholamine and/or potassium. There is a possibility that these substances might also affect the AT.

Adolescent↗
PubMed1991

Cardiorespiratory responses to cyclic triangular ramp forcings in work load.

The dynamic responses of minute ventilation, heart rate, cardiac output, oxygen uptake, and carbon dioxide output to cyclic ramp exercise were studied on six healthy male subjects. Exercise was performed in the sitting position using a cycle ergometer. On separate occasions, three different ramp slopes, i.e. 33.3 (repeated for three cycles), 20 (two cycles), and 14.3 W/min (one cycle), were applied over the load range from 0 to 100 W. Mean response times (MRTs) were determined by adopting an exponential function with a time delay to the transient responses. The MRTs of the ascending phase of the first cycle were elongated with a decreasing ramp slope in almost all variables, while those for the descending phase remained unchanged. This resulted in notable asymmetry of the responses in the first cycle. However, there was negligible asymmetry observed in subsequent cycles and the MRTs gradually attained their proper values. Asymmetry in cardiac output was less noticeable compared with that of the respiratory variables. The correlation between the MRTs for ventilation and carbon dioxide output was highly significant, suggesting that a cardiodynamic or humoral mechanism may be related to this phenomenon.

Adult↗
PubMed1989

Cardiodynamic factors affecting hyperpnea during steady-state exercise in man.

In order to know the role of cardiodynamic factors for exercise hyperpnea, ventilation and several cardiorespiratory variables were measured simultaneously in human subjects during exercise. Cardiac output (Q) and mixed venous CO2 content (CVCO2) were determined by a rebreathing method. The correlation coefficients (r) for the relationships between minute expiratory ventilation (VE) and each of end-tidal CO2 tension (PETCO2), Q, CVCO2, CO2 flow into the lung (QCO2, the product of Q and CVCO2), oxygen consumption (VO2), and CO2 output (VCO2) were determined during the steady-state exercise up to 90 W. The correlation was highly significant (r = 0.84-0.99, p less than 0.001) in each case except for PETCO2 (r = 0.13, N.S.). The highest correlation was observed in the VE-VCO2 relationship. It was assume that VCO2 released from the pulmonary capillaries into the alveoli is the most likely stimulus leading to exercise hyperpnea. Arterial CO2 oscillation may be regarded as a potential linkage between VCO2 and VE.

Adult↗
PubMed1989

A comparison between cardiac output determined by impedance cardiography and the rebreathing method during exercise in man.

Cardiac output was determined by impedance cardiography (Q(imp)) and a rebreathing method (Q(reb)) during exercise of loads up to 90 W. The correlation between Q(imp) and Q(reb) was generally good, but it was found in two of four subjects that Q(imp) was slightly lower than Q(reb) at the higher exercise levels. The regression equation for both Q values was: Q(imp) = 0.91 Q(reb) + 0.25 (l/min, r = 0.87, p less than 0.001).

Adult↗
PubMed1988

Estimation of the transfer coefficients of oxygen and carbon monoxide in the boundary of human and chicken red blood cells by a microphotometric method.

The reaction rates of O2 and CO with the human and chicken red blood cell (RBC) were measured by using a microphotometric apparatus. In the experiments on the human RBC, a small amount of RBCs were put in an air-tight reaction cuvette. Gas mixtures containing various concentrations of O2 and CO were sequentially injected into the cuvette and the change in O2 and CO saturation of hemoglobin was measured from the change in transmission of the RBCs at 402 and 416.5 nm. The reaction rate of CO with RBCs was significantly influenced by photodissociation of carboxyhemoglobin (COHb). To eliminate this, a short-pass filter (400 to 435 nm) and a sector (100 Hz) were used. By comparing the measured reaction rates of O2 and CO with the theoretical rates obtained from the numerical solutions of the partial differential equations of the diffusions of O2 and CO, the transfer coefficients of O2 and CO (eta O2 and eta CO) in the RBC boundary, including the RBC membrane and water layer around the RBC, were estimated. Both the values showed good agreement, ranging from 0.3 to 2.5 x 10(-6) cm.sec-1.Torr-1. Furthermore, the chorioallantoic capillary of chicken embryo was used for the measurements of the reaction rates of O2 and CO with RBC through the capillary membrane. The reaction rates of O2 and CO in the chorioallantoic capillary were slower than those obtained in the human RBC. By comparing the measured reaction rates and the numerical solutions, the eta O2 and eta CO in the boundary, including the capillary membrane, plasma, and RBC membrane, were estimated. These two values ranged from 0.1 to 0.4 x 10(-6) cm.sec-1.Torr-1 and showed good agreement. These results suggest that the diffusion rates for O2 and CO across the capillary and RBC membrane are similar.

Animals↗
PubMed1987

One-sampling rebreathing method to measure diffusing capacity for CO.

To simplify the rebreathing method to obtain the pulmonary diffusing capacity for CO (DLCO), a one-sampling method was developed, combined with a simulation technique. The change in CO fraction in rebreathing air depends on the rebreathing volume (VRB), the dead space volume (VD), the gas volume in the lung-bag-system (VS) as well as the DLCO: Using the measured VRB, VD, and VS, the changes in CO fraction in bag and alveolar air were simulated by varying the DLCO, where the expired and inspired gas volumes were represented by a sinusoidal function of time. The DLCO was determined by checking the similarity between the simulated and measured CO fractions at the 7th expiratory period. To confirm the validity of the simulation method, two-sampling rebreathing and single breath methods were additionally carried out in 6 normal subjects in the sitting position. The DLCO measured by the simulation agreed well with that measured simultaneously by the two-sampling method. The DLCO measured by this method was also compatible with that obtained from the single breath method, when the dead space was excluded from the measured lung gas volume.

Adult↗
PubMed1986

Evaluation of uneven distribution of VA/Q ratio from data on exchange of respiratory gases.

A new approach has been developed for evaluating uneven distribution of ventilation/perfusion ratio, VA/Q, based on a two-compartment model with a reciprocal VA/Q relation. The VA/Q ratios were expressed by mu . (1-rho)/rho and mu . rho/(1-rho), where mu and rho were referred to as the "ideal" VA/Q ratio and unevenness factor, respectively. During steady state breathing, arterial blood was analyzed for PO2 and PCO2, and end-tidal PCO2 as well as the gas exchange ratio, R, was measured. After steady state breathing a rebreathing experiment was performed, and the arterial-venous O2 content difference, (a-v)CO2, was measured, and then, multiplying it by R, the venous-arterial CO2 content difference, (v-a)CCO2, was obtained. Referring to these values the mixed venous PO2 and PCO2 were estimated from arterial PO2 and PCO2, using the O2 and CO2 dissociation curves. The VA/Q line and iso-R line were drawn to find mu, and further, total arterial, and alveolar PO2 and PCO2 of the two-compartment model were computed by changing both rho and the mixing weight factor, phi. The phi value was determined so as to make the above PO2-PCO2-locus pass through the measured arterial PO2 and PCO2. The rho value was selected so that the computed alveolar PCO2 fitted to the end-tidal one. The experiments were performed on 8 normal subjects in normoxia and hyperoxia with PIO2 245 Torr. The mean phi values in normoxia and hyperoxia were 0.50 and 0.56, respectively. The mean rho values in normoxia and hyperoxia were 0.438 and 0.428, respectively. The VA/Q ratio was decreased in hyperoxia because of a decrease in VA value.

Carbon Dioxide↗
PubMed1986

Change in O2 uptake during rebreathing in hyperoxia in man.

In pertaining to PO2 dependency of the pulmonary CO diffusing capacity during rebreathing, the O2 uptake (VO2) and cardiac output (Q) were measured at three different PO2 levels between 100 and 500 Torr. Since the VO2 measured by an O2 injection method is strongly influenced in hyperoxia by a gas exchange ratio (R), a simulation method using a R-PCO2 relation during rebreathing was developed. Gas volume in the lung-bag-system needed in the computation was measured from the difference in O2 concentration between before and after injecting a known amount of O2 into the rebreathing circuit. The accuracy of the volume was checked by comparing it with the volume measured successively with a body box. The VO2 was determined by comparing the simulated O2 and CO2 concentrations in rebreathing gas with the measured ones. The VO2 significantly increased by rebreathing in hyperoxia. To analyze the VO2 increase, the Q was computed by dividing the VO2 by the arteriovenous O2 content difference, which in turn was obtained by dividing the slope of the CO2 dissociation curve by that of the R-PCO2 line. The Q was almost linearly related to the VO2. Since there was no difference in VO2 in steady state breathing between normoxia and hyperoxia, the increase in VO2 and Q seemed to occur transiently. This finding is very important in evaluating the PO2 dependency of the pulmonary diffusing capacity for CO.

Adult↗
PubMed1984

An epidemic study of molluscum contagiosum. Relationship to swimming.

The incidence of molluscum contagiosum (MC) in children attending 15 public elementary schools and 9 kindergartens in Chigasaki City was studied by questioning their parents. Special attention was paid to the relationship between MC and swimming, and the incidence of MC in the swimming group was twice as high as that of the nonswimming group. This study also revealed that the predilection for lesions was the side of the trunk and the axillae.

Child↗
PubMed1984

Secondary CO2 diffusion following HCO3- shift across the red blood cell membrane.

In order to clarify the interaction between CO2 diffusion and HCO3- shift in the red blood cell (RBC), HCO3- shift was measured by using a stopped flow method combined with fluorometry. When HCO3- entered the RBC, the intracellular PCO2 increased, causing a secondary outflow of CO2. Conversely, when HCO3- ions flowed out of the RBC, the resulting decrease of PCO2 caused an inward CO2 diffusion. The PCO2 change caused by the inward HCO3- shift was about 3- to 4-fold that of the outward shift. During the respective in- and outward-shifts, the mean half-times of the extracellular pH changes were 0.15 and 0.13 sec. These were approximately twice as long as those of the primary CO2 diffusion. The permeability of HCO3- across the RBC membrane was obtained by comparing the experimental extracellular pH curve with a numerical solution for CO2 and HCO3- diffusions accompanied by the hydration and dehydration reactions. Thus the HCO3- permeability was determined to be 5 x 10-4 cm/sec, in the in- and outward-HCO3- shifts, respectively. The influence of Cl- concentration on HCO3- permeability was tested by reducing the initial Cl- gradient across the RBC membrane. In a physiological Cl- concentration range the HCO3- permeability was not affected by the Cl- gradient.

Bicarbonates↗
PubMed1984

Change in PCO2 in red cell suspension following bicarbonate shift.

To reveal the CO2 diffusion process into and out of the red blood cell (RBC), changes in PCO, following the HCO3- shift were examined. The RBC suspension was mixed at 37 degrees C with saline solution having different HCO3- concentrations. In proportion to the intracellular HCO3- change caused by the HCO3- shift, the PCO2 change was increased. The rate of change increased as the hematocrit and the initial intracellular HCO3- content decreased. For calculating the above PCO2 change, a theoretical equation was derived from the Henderson-Hasselbalch equation and the relation between both the changes in buffer base and intracellular pH. The calculated PCO2 change coincided well with the measured value, suggesting the validity of the theoretical equations.

Adult↗
PubMed1984

A new indirect method for measuring arteriovenous O2 content difference and cardiac output from O2 and CO2 concentrations by rebreathing air.

A new indirect method for measuring the arteriovenous O2 content difference (avDO2) was developed. The avDO2 was calculated by dividing the gradient of the CO2 dissociation curve by that of a gas exchange ratio against PCO2. The latter slope was obtained from O2 and CO2 concentrations in rebreathing air. The validity of the method was tested preliminarily in human subjects by comparing the cardiac output calculated from avDO2 and O2 uptake (VO2) with that measured hitherto by other authors, and then in dogs by comparing the calculated avDO2 with the measured value. In the dog experiments, the rebreathing was performed 7 times in each of 7 dogs. Immediately after the rebreathing arterial and mixed venous blood were sampled and analyzed for avDO2. For each rebreathing period the avDO2 was calculated by using the CO2 dissociation curve obtained in the individual dogs. The correlation coefficient between the measured and calculated avDO2 was 0.87, demonstrating reasonable validity of the method. The VO2 was further measured from the time interval during which a known amount of pure O2 was consumed. Then, the cardiac output was calculated by dividing the VO2 by the measured and calculated avDO2. The correlation coefficient between the respective cardiac output values was 0.88, indicating the reliability of using the calculated avDO2.

Animals↗
PubMed1983

Relationship between hematocrit and CO2 contents in whole blood and true plasma.

The amount of CO2 liberated out of the red cell was measured by decreasing PCO2 in human blood with different fractional hematocrits of about 0.24, 0.45, and 0.75, respectively, in order to elucidate whether it depends on the hematocrit and the intracellular pH. From a venous PCO2 level the PCO2 of the sample blood was lowered to 12 Torr. PCO2, CO2 content, pH, Cl-, and Na+ were measured in whole blood and true plasma before and after the reduction of PCO2. Change in water concentration in plasma was calculated from change in plasma Na+ concentration. The bicarbonate shift well counterbalanced to the Cl- shift. As the hematocrit was decreased, the amount of CO2 released per mol of hemoglobin increased, while the change in intracellular bound CO2 concentration decreased. That is, the intracellular bound CO2 became higher in the lower hematocrit blood than in the higher hematocrit one. This fact suggested that the intracellular pH became higher as the hematocrit was lowered, and thus the amount of alkali bound with hemoglobin or the CO2 release was enhanced. The Donnan ratio of the bound CO2 at 12 Torr was independent of the hematocrit, though the pH was inversely related to the hematocrit.

Adult↗
PubMed1983

Diffusion coefficients of CO2 molecule and bicarbonate ion in hemoglobin solution measured by fluorescence technique.

The diffusion process of CO2 within a thin layer of hemoglobin (Hb) solution was followed by pH-sensitive fluorescence of 4-methylumbelliferone. In the presence of sufficient carbonic anhydrase in the layer, the pH change was accelerated and determined only by the diffusion. The diffusion rate was reduced as the Hb concentration was increased. The pH rise observed in the CO2 diffusion out of the layer was slower than the pH fall caused by inward diffusion. However, the outward diffusion rate was faster than the inward diffusion rate in contrast to the pH change. The diffusion coefficients of molecular CO2 and bicarbonate ion were separately determined from the simulated and experimental PCO2-time curves by utilizing the non-linearity of the CO2 dissociation curve. The simulated curve was obtained from a numerical solution of the differential equation for diffusion by using the measured CO2 dissociation curve. The diffusion coefficient of CO2 was assumed to decrease exponentially with increasing Hb concentration. The diffusion coefficient of HCO3- was found to be reduced hyperbolically as the Hb concentration was increased. The diffusion coefficients of CO2 and HCO3- of 100% hemolysate were 0.34 X 10(-5) and 0.14 X 10(-5) cm2/sec, respectively.

Adult↗
PubMed1983

Rate of CO2 diffusion in the human red blood cell measured with pH-sensitive fluorescence.

The diffusion rate of CO2, into and out of the red cell, was measured by using a stopped flow method with pH-sensitive fluorescence of 4-methylumbelliferone. A red cell suspension of 15% hematocrit with the PCO2 of 8 Torr (or 65 Torr) was mixed with the same amount of saline solution having 65 Torr (or 8 Torr). Carbonic anhydrase was added to the external solution at a concentration of 20 mg/100 ml in order to accelerate the hydration and dehydration reactions, so that the PCO2 change in the fluid could be observed instantaneously through pH. In the inward diffusion PCO2 showed a large change, suggesting a lack of HCO3- shift across the red cell membrane. In the outward diffusion, however, the PCO2 change was smaller, suggesting that H+ ions produced in the external solution by CO2 hydration were rapidly buffered by the red cell. The half-times of the inward and outward diffusions were, on an average, 0.08 and 0.13 sec, respectively. The results of the simulation revealed that the above difference in half-times was attributed to the difference in slope between the two dissociation curves with and without the HCO3- shift. The diffusion rate was almost constant and remained independent of the direction of CO2 flux. That is, at a low pH range the permeation of H+ ions across the red cell membrane was much faster than the diffusion rate of CO2.

Carbon Dioxide↗
PubMed1981

The influence of the Haldane effect on alveolar CO2 tension equilibrated with mixed venous blood in man.

When blood in the pulmonary capillary is oxygenated in hypercapnic air, PCO2 in the red cell has been thought to exceed alveolar PCO2 due to the Haldane effect, inducing outward CO2 diffusion. As long as the inward CO2 diffusion and, consequently, HCO3- formation are prevented in the red cell, the CO2 gain in plasma is reduced down to the level predicted from a CO2 dissociation curve of separated plasma. Therefore, if the direction of the CO2 diffusion is not reversed during the contact time, the virtual venous PCO2 (PEq), where the CO2 loss due to the Haldane effect is balanced with the gain due to the venoalveolar PCO2 gradient, becomes higher than the oxygenated venous PCO2 in proportion to the CO2 difference between the true and separated plasma. In order to verify the validity of the above assumption, the PEq value was measured in normo- and hypercapnia by using the Defares' extrapolation method in six normal subjects. The results obtained revealed that the PEq estimated in hypercapnia was obviously higher than that in normocapnia. The above difference was significantly greater in normoxia than in hypoxia. Furthermore, it agreed fairly well with the theoretical difference presumed by taking the difference in CO2 content between separated and true plasma and the R. Q. effect on the alveolar gas volume into account, suggesting that the inward CO2 diffusion following the oxygenation reaction could be disregarded in normoxic hypercapnia.

Adult↗