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Biomedical subjects

A Kamiya

Publications and source records attributed to A Kamiya.

At least 163 records · Page 9Linked to original sources
PubMed1990

The efficiency of the vascular-tissue system for oxygen transport in the skeletal muscles.

The efficiency of the vascular-tissue system for oxygen (O2) transport in the skeletal muscle was estimated by using Krogh's cylinder model for the capillary-tissue arrangement. The tissue mass supplied by a single capillary was calculated as the region of positive O2 tension. For given values of total muscle flow and tissue O2 consumption rate, total tissue mass was determined as the function of the capillary number (n). The energy cost to maintain the vascular system with n terminals (capillaries) was assessed by the minimum volume model by Kamiya and Togawa (1972). The efficiency of the entire system was evaluated by calculating the ratio of (total tissue mass) or (total O2 consumption)/(the energy cost). The results of the calculation using physiological data of muscle blood flow and O2 consumption rate in man during exercise revealed the optimum capillary number to be around 1.5 x 10(10) and the Krogh cylinder radius to be 26 microns, which agrees well with the morphological data of these values in human skeletal muscles. It was concluded that the vascular-tissue system in the skeletal muscle is constructed so as to attain the highest efficiency in O2 transport to tissue during exercise.

Animals↗
PubMed1990

Fluid shear stress enhanced DNA synthesis in cultured endothelial cells during repair of mechanical denudation.

We have previously observed a stimulatory effect of fluid shear stress on the regeneration of cultured endothelial cell layers after mechanical denudation. In this study we examined how fluid shear stress affects endothelial cell DNA synthesis during regeneration. Following mechanical denudation of narrow linear areas, monolayers of bovine aortic endothelial cells cultured on plastic dishes were subjected to shear stress of 1.3-4.1 dynes/cm2 for 24-48 hours in a specially designed apparatus. After the application of shear stress, cells were stained with propidium iodide, and its fluorescence intensity, reflecting cellular DNA content, was measured using photometric fluorescence microscopy. The DNA content of cells exposed to shear stress increased significantly more than that of paired, static control cells (p less than 0.005 to p less than 0.001). The DNA histogram showed that cells exposed to shear stress contained a relatively high proportion of cells located in the S, G2, and M phases of the cell cycle as compared with the static control. These data suggest that fluid shear stress enhances endothelial cell DNA synthesis during the repair of mechanical denudation.

Animals↗
PubMed1990

[Fluid shear stress effects on intracellular calcium concentrations in cultured vascular endothelial cells].

Vascular endothelial cells are known to modulate their functions in response not only to humoral stimuli but also to such physical stimuli as fluid shear stress generated by blood flow. However, the mechanisms by which the hemodynamic force acts on endothelial cells are not yet well understood. We have studied how endothelial cells recognize the shear stress and mediate it to intracellular organelles. Cultured monolayers of bovine aortic endothelial cells loaded with the highly fluorescent Ca+(+)-sensitive dye Fura 2 were exposed to different levels of fluid shear stress in a specially designed flow chamber and simultaneous changes in intracellular-free Ca+(+) concentration were measured using photometric fluorescence microscopy. Application of shear stress to cells by fluid perfusion led to an immediate several-fold increase in Ca+(+) concentration within 1 min, followed by a rapid decline, and finally a plateau somewhat higher than control levels during the entire period of the stress application. The early part of the response, but no plateau, was observed even in Ca+(+)-free medium added with 2 mM EDTA, and in the presence of calcium antagonists (e.g. 2 x 10(-5) M nicardipine). Thus, endothelial cells may have a flow-sensing property which recognize the shear stress on the membrane as a stimulus and mediates the signal to increase intracellular free Ca(+)+ which is a major component of the internal signalling system of the cell.

Animals↗
PubMed1989

The mutagenicity of refuse leachate from a municipal incinerator.

The mutagenicity of refuse leachate from a municipal incinerator was studied by liquid rec-assay and Ames assay. Volatile components were found to be negative, and nonvolatile components positive, in the Ames assay and the leachate was found to have DNA-damaging capacity in the liquid rec-assay with S-9 mix. PAHs derived from tobacco ash and carbonyl compounds generated by the putrefaction of foods were confirmed to be main contributors to DNA-damaging capacity and mutagenicity in refuse leachate.

Animals↗
PubMed1989

Contribution of monoamine oxidase (MAO) to the binding of tertiary basic drugs in lung mitochondria.

The effects of tertiary amine-containing basic drugs on the enzymes located in the mitochondria and the effect of monoamine oxidase inhibitors (MAOIs) on drug accumulation in lung mitochondria have been studied. Various basic drugs inhibited MAO activity but not other mitochondrial marker enzymes. The potency of MAO inhibition correlated well with their lipid solubility, and the basic drugs inhibited MAO activity dose dependently and competitively. Further, MAO inhibition correlated well with binding affinity to lung mitochondria, and the binding of tertiary amine drugs to lung mitochondria was decreased by treatment with MAOIs. A good correlation was observed between the potency of MAOIs to inhibit the binding of the basic drug to the high-affinity site in mitochondria and the MAO inhibitory activity in mitochondria. These results indicate that mitochondrial MAO is one of the binding sites for tertiary basic drugs in the lung. We think that the action and/or adverse reaction of some drugs may result from inhibition of mitochondrial MAO to metabolize various biogenic amines and that mitochondrial MAO may function as a reservoir for basic drugs.

Animals↗
PubMed1989

Pharmacokinetics and dromotropic activity of ajmaline in rats with hyperthyroidism.

1. The pharmacokinetics and the dromotropic action (increased PQ interval) of intravenously administered ajmaline (2 mg kg-1) were studied in hyperthyroid rats with sinus tachycardia. The hyperthyroidism was induced by intraperitoneal injection of 3,5,3'-triiodo-L-thyronine (0.5 mg kg-1) for 4 days. 2. The change in the ajmaline concentration in whole blood could be described by a biexponential equation. The steady state distribution volume of ajmaline decreased from 4.81 l kg-1 in control rats to 3.80 l kg-1 in hyperthyroid rats and the total body blood clearance was slightly higher in hyperthyroid rats than in control rats. 3. Ajmaline exhibited a saturable binding to rat plasma proteins, and one kind of binding site was found in the observed range of concentrations. The binding capacity was 2 fold higher in hyperthyroid rats than in control rats. 4. On the basis of the plasma unbound concentration, ajmaline exhibited an increased negative dromotropic activity in hyperthyroid rats compared with control rats. 5. A positive correlation was found between the pacing rate and the dromotropic action of ajmaline on atrioventricular conduction in isolated perfused hearts. There was no significant difference in the rate-dependence of the effect of ajmaline on the heart between control and hyperthyroid rats. 6. Our findings suggest that the increased dromotropic activity of ajmaline is mainly due to the increased heart rate in hyperthyroid rats.

Ajmaline↗
PubMed1989

Submitochondrial distribution of basic drugs in the isolated perfused lung.

To clarify the mechanism by which basic drugs accumulate in the lung mitochondria, the binding selectivity of drugs to different submitochondrial components of the perfused rat lung was examined. The accumulation of basic drugs was the highest in the mitochondrial outer membrane fraction. The drug accumulation in this fraction increased with lipid solubility and was dose-dependent. It appears then that selective binding sites for basic drugs are present in the mitochondrial outer membrane.

Animals↗
PubMed1989

Accumulation mechanism of basic drugs in the isolated perfused rat lung.

The mechanism of the accumulation of basic drugs was investigated by isolated rat lung perfusion. Treatment with various metabolic inhibitors or non-basic drugs did not affect the accumulation of a basic drug in the lung, but a second basic drug inhibited the accumulation of the first basic drug depending on its lipid solubility. The basic drug already accumulated was rapidly displaced by the second drug except for poorly lipid-soluble basic drugs and non-basic drugs. The ability of a second basic drug to displace the first basic drug was well correlated with its ability to inhibit accumulation. From the Scatchard plot, at least two independent sets of binding sites for basic drugs were found to be present in the isolated perfused lung. The maximum binding capacity for each basic drug was similar in both sites. These results indicate that specific common binding sites for basic drugs, which do not contribute to the active transport system, exist in the lung tissues and the affinity to the sites depends on the lipid solubility of the basic drugs.

Animals↗
PubMed1989

[Measurement of changes in distance between the femoral and the tibial drill holes for the anterior cruciate ligament reconstruction].

We have developed an experimental system in which a new Gallium-Indium containing transducer can continuously measure the changes of separation distances between the femoral and tibial points. The measurements provides information for the attachment location in the anterior cruciate ligament (ACL) reconstruction and used for various combinations of extra-articular and intra-articular methods. At the first experiment, the distance between each pair of points at the level of the capsule for fifteen combinations during simple flexion-extension knee motion were measured on six cadaveric knees. At the next experiment, in an ACL-deficient knee the distances of ten combinations in the intra-articular method were measured. These results indicated that for an isometric placement the combination of the center of tibial insertion and the postero-proximal of the femoral origin of the ACL appeared to furnish a better location for intraarticular reconstruction. No combination was recommended for extraarticular reconstruction.

Biomechanical Phenomena↗
PubMed1988

Isolation of dinitropyrene in emission gas from a municipal incinerator and its formation by a photochemical reaction.

In a previous paper, direct-acting mutagenicity was reported in emission gas from incomplete municipal incineration using Salmonella typhimurium TA-98 and TA-100. This paper reports the detection of dinitropyrene (DNP) as a direct-acting mutagen using nitrogen selective gas chromatography. The gas-phase photochemical reaction of pyrene with nitrogen dioxide was examined in a quartz vessel with various reaction times and temperatures. 1-Nitropyrene (1-NP) was readily formed from pyrene in the absence of light irradiation and at low temperature, but DNP was not formed under similar conditions. DNP formation was catalyzed by nitric acid. The formation of DNP is dependent on light irradiation, temperature and HNO3 as catalyst. In a combustion source these factors affect the formation of DNP.

Air Pollutants↗
PubMed1988

Moment analysis of drug disposition in kidney: transcellular transport kinetics of p-aminohippurate in the isolated perfused rat kidney.

The mean renal epithelial cell residence time, Tcell, was defined as a model-independent characteristic of the transcellular transport process in the isolated perfused kidney. The transcellular transport process includes transport at the basolateral membrane, diffusion in the cytosol, and transport at the brush border membrane. The parameter Tcell represents the mean time for the drug secreted from the tubules to pass through the renal epithelial cells, and is calculated as the difference of the mean urinary transit time between secreted drug and inulin in the single-pass perfusion system. Therefore, the urinary excretion rate-time course is indispensable to evaluate Tcell. p-Amino-hippuric acid was used as a model compound. The bovine erythrocytes in the perfusate kept the isolated kidney in an almost constant physiological condition, including secretion function. The renal vein outflow curves were also analyzed by the use of moments. The dispersion in the catheter was corrected by a deconvolution. The apparent secretion intrinsic clearance and the apparent volume of distribution were calculated from the moments. The present method will be useful for analysis of the transcellular transport mechanism and the effect of disease states on renal transport of drugs.

Aminohippuric Acids↗
PubMed1988

Cytoplasmic calcium response to fluid shear stress in cultured vascular endothelial cells.

Vascular endothelial cells modulate their structure and functions in response to changes in hemodynamic forces such as fluid shear stress. We have studied how endothelial cells perceive the shearing force generated by blood flow and the substance(s) that may mediate such a response. We identify cytoplasmic-free calcium ion (Ca++), a major component of an internal signaling system, as a mediator of the cellular response to fluid shear stress. Cultured monolayers of bovine aortic endothelial cells loaded with the highly fluorescent Ca++-sensitive dye Fura 2 were exposed to different levels of fluid shear stress in a specially designed flow chamber, and simultaneous changes in fluorescence intensity, reflecting the intracellular-free calcium concentration [( Ca++]i), were monitored by photometric fluorescence microscopy. Application of shear stress to cells by fluid perfusion led to an immediate severalfold increase in fluorescence within 1 min, followed by a rapid decline for about 5 min, and finally a plateau somewhat higher than control levels during the entire period of the stress application. Repeated application of the stress induced similar peak and plateau levels of [Ca++]i but at reduced magnitudes of response. These responses were observed even in Ca++-free medium. Thus, a shear stress transducer might exist in endothelial cells, which perceives the shearing force on the membrane as a stimulus and mediates the signal to increase cytosolic free Ca++.

Animals↗
PubMed1988

Urinary excretion and diuretic action of furosemide in rats: increased response to the urinary excretion rate of furosemide in rats with acute renal failure.

A urinary excretion-response curve representing the urinary excretion rate of furosemide versus the urinary excretion rate of (Na+ + K+) was used to analyze furosemide action in rats with uranyl nitrate-induced acute renal failure (ARF) with and without dopamine coadministration. Urinary excretion of furosemide, but not its serum concentration, was the determinant for the diuretic action of furosemide. Increased diuretic response was observed in ARF rats, although the total diuretic response and urinary recovery of furosemide within 2 hr decreased. Dopamine enhanced furosemide-induced diuresis in ARF rats in terms of the total urine output and urinary electrolyte excretion, although the urinary excretion-response curves were not different. This enhancement by dopamine was found to be caused by the augmented urinary excretion of furosemide and the increased response to this drug in ARF rats. These findings suggest the contribution of decreased concentrating ability along the nephron and/or increased sensitivity of cells at the site of action to this drug.

Acute Kidney Injury↗
PubMed1988

A quantitative method of evaluating the diuretic response to furosemide in rats.

Furosemide effects are usually evaluated by measuring the urinary excretion rate of Na+ (UVNa) in humans. In the present study, however, UVNa showed a nonlinear relationship with urine flow rate after intravenous injection of furosemide in rats. In contrast, when the urinary excretion rate of (Na+ + K+) (UVNa + K) was plotted against the urine flow rate, a linear regression line was observed, with small interindividual variations in normal rats and in rats with uranyl nitrate-induced acute renal failure (ARF). Piretanide, a loop diuretic, also showed a similar relationship, while other types of diuretics revealed different slope values for the relationship. Although the urinary excretion rate of Cl- (UVCl) vs UVNa + K is expected to show a linear relationship in normal rats, the correlation coefficient of the linear regression line was smaller than that of the urine flow rate vs UVNa + K. Further, the slope of UVCl vs UVNa + K was slightly different in ARF rats. Therefore, UVNa + K provides a better quantitative measure of diuretic response to loop diuretics than UVNa or UVCl.

Acute Kidney Injury↗
PubMed1988

Increased diuretic response to furosemide in rats with glycerol-induced acute renal failure.

To clarify the diuretic response to furosemide in a diseased state, the urinary excretion of furosemide, water, and electrolytes was examined after a single intravenous injection of furosemide in control rats and rats with mild acute renal failure (ARF) induced by glycerol. The urinary recovery of furosemide was similar in the control and ARF rats. However, the diuretic response to furosemide was increased in ARF rats compared with control rats. Although the relationship between the urine flow rate (UFR) and the urinary excretion rate of (Na+ + K+) (UV Na + K) was the same in both groups, the urinary excretion rate of K+ (UV K) was decreased in ARF rats. The concentrating ability in ARF rats was also decreased compared with that in control rats. By infusion of aldosterone in ARF rats, both UV K and the concentrating ability were increased and the diuretic response to furosemide was decreased, whereas the relationship between UFR and UV Na + K was not changed. Therefore, it is concluded that the increased diuretic response to urinary excretion of furosemide in ARF rats may be caused, at least in part, by the decreased concentrating ability along the nephron.

Acute Kidney Injury↗
PubMed1988

Decreased diuretic response to furosemide in rats with acute hepatic failure.

Furosemide diuresis is occasionally reduced in cirrhotic patients with ascites. To define this phenomenon, the amounts of water, electrolytes, and furosemide excreted in urine were measured in control and CCl4-induced acute hepatic failure (AHF) rats. The diuretic action of furosemide (10 mg/kg, i.v.) was reduced in AHF rats, accompanied by increased plasma aldosterone concentration and accelerated urinary K+ excretion rate. Furosemide transiently increased the urinary inulin excretion rate (UVIN) in both control and AHF rats. Then the UVIN quickly returned to the baseline value in control rats, but rapidly dropped below the baseline in AHF rats. To clarify the contribution of aldosterone in these phenomena, AHF rats was adrenalectomized (ADX) and treated with or without exogenous aldosterone. The UVIN in ADX rats given no infusion or a low-dose aldosterone infusion was similar in pattern to that of the control group, but the UVIN in the ADX rats given a high-dose aldosterone infusion showed a pattern similar to that of the AHF rats not adrenalectomized. These findings indicate that an increase in plasma aldosterone concentration is an important factor responsible for the decreased diuretic action of furosemide, along with the reduced glomerular filtration rate.

Adrenalectomy↗