Biomedical subjects

K Katayama

Publications and source records attributed to K Katayama.

At least 415 records · Page 23Linked to original sources

PubMed1988

Temporal Fourier transform of digital angiograms for left ventricular regional wall motion analysis.

To determine whether or not the first harmonic of a temporal Fourier transform, applied pixel-by-pixel on time-intensity curves, can detect the subtle wall motion abnormalities due to ischemia, 6 dogs were instrumented with a micromanometer in the left ventricles, a hydraulic cuff occluder around the circumflex coronary artery, and sonomicrometers on the inferior (ischemic) and anterior (non-ischemic) walls. Left ventricular images, obtained after contrast injection via the pulmonary artery, were compared with dimension signals in control and 3 progressive levels of coronary stenosis (Stenosis I, II and III). Normalized, digital functional images (512 x 512 matrix, 256 shades of gray/pixel) were divided into anterior, apical, and inferior areas to acquire regional mean phase (degrees) and amplitude (intensity units) values. After inducing stenosis, phase in ischemic region significantly increased at all 3 levels of stenosis, whereas amplitude significantly decreased at Stenosis II and III. However, amplitude images showed clearly the topographic site of ischemia. There was a progressive increase in phase and decrease in amplitude in ischemic areas as the percent wall thickening (%WTh) fell (phase vs. %WTh: r = -0.55, p less than 0.005; amplitude vs. %WTh: r = 0.71, p less than 0.001). Heart rate and peak systolic pressure showed no significant changes during stenosis. We conclude that quantitative functional images, generated from a temporal Fourier transform, are sensitive to the detection of left ventricular regional wall motion abnormalities during mild, moderate, and severe degrees of ischemia.

Animals↗

PubMed1988

Catecholamine and thyroid hormone metabolism in a case of anorexia nervosa.

Alterations in catecholamine (CA) and thyroid hormone metabolism were examined in a 12-year-old girl with anorexia nervosa during 3 months of treatment. According to her body weight change, the observation period was divided into 3 stages: initial emaciation (stage 1), stable maintenance of the -30% level of the previous weight (stage 2) and convalescent stage (stage 3). Stage 1 was characterized by relatively high urinary norepinephrine (NE) and epinephrine (E) but low dopamine (DA) excretion, elevated plasma DA-beta-hydroxylase (DBH) activity and reduced serum thyroid hormones, especially the triiodothyronine (T3) level. In stage 2, urinary CAs were markedly suppressed, while serum thyroid hormones gradually increase. In stage 3, a great increase in DA excretion, a fall in plasma DBH activity and normalization of thyroid hormones were observed. In the low T3 state below 60 ng/dl, urinary NE + E/DA ratios were elevated and widely fluctuated (0.58 +/- 0.30, SD), but were gradually decreased and completely stabilized in the normal T3 state (0.07 +/- 0.02, P less than 0.001). These results indicate that (1) although total CA production was depressed in anorexia nervosa, a change from an adrenergic-dominant to a dopaminergic-dominant state occurs in accordance with body weight gain, and (2) this shift in the CA profile is associated with concomitant recovery of reduced thyroid hormone concentrations. Thus, as for the energy expenditure, compensatory changes were observed in CAs and thyroid hormones in relation to caloric restriction.

Anorexia Nervosa↗

PubMed1988

[Effect of PMU therapy (CDDP, MMC and UFT) against terminal gastric carcinoma. Hokuriku Cisplatin Round-table Conference].

PMU therapy with 75 mg/m2 of CDDP, 10 mg/body of MMC and 400 mg/day of UFT was performed on 57 patients with terminal gastric carcinoma. The treatment resulted in CR in 2, PR in 9, MR in 1, NC in 16 and PD in 9 of 37 patients with evaluable cases, with a response rate of 30% (11/37 patients). In the 11 responders, the mean disease-free interval was 6.6 months with a median interval of 5 months, and the mean survival period was 9.2 months with a median survival period of 6 months, while in the 46 non-responders, the mean survival period was 6.7 months with a median survival period of 5 months. In all patients, the mean survival period was 7.1 months with a median survival period of 6 months. Adverse reactions to the treatment included gastrointestinal disturbance observed in 77%, nephrotoxicity in 14%, and myelotoxicity in 26% of the patients, but all reactions became normalized during the course of observation. These results have led to the conclusion that PMU therapy may be an effective treatment for terminal gastric carcinoma.

Adult↗

PubMed1988

[A case of disappearance of peritoneal dissemination in gastric cancer induced by continuous hyperthermic peritoneal perfusion with cisplatin and mitomycin C].

A 58-year-old woman who had undergone subtotal gastrectomy for advanced gastric cancer yielded massive ascites after 6 months. The cytology of ascites showing Class V indicated recurrence of peritoneal dissemination in the gastric cancer. Since laparotomy disclosed diffusely small tubercular seedings in all areas of the peritoneal cavity, she received continuous hyperthermic peritoneal perfusion (CHPP) with 300 mg Cisplatin and 30 mg Mitomycin C. After CHPP ascites disappeared for 4 months. Macroscopically and microscopically, there was no cancerous lesion in the peritoneal cavity by following second-look operation. This result encouraged us to try therapeutic CHPP for overt peritoneal dissemination.

Ascitic Fluid↗

PubMed1988

[Experimental mitral regurgitation in ischemia-induced papillary muscle dysfunction].

Mitral regurgitation (MR) reportedly develops by ischemia of the papillary muscles, which is called papillary muscle dysfunction. This report deals with the roles of papillary muscles and left ventricular walls on the pathogenesis of MR using graded injuries of these structures in 23 dogs. Implanted ultrasonic microcrystal and occluder with an electromagnetic flowmetry for the left circumflex coronary artery were the main experimental setting. Graded occlusion of the artery was done by the six-step approach regarding coronary blood flow (CBF) reduction (C1-C6). Left ventricular (LV) pressure, systolic thickening (%W: sonomicrometry) of the LV anterior (AW) and posterior walls (PW), and systolic longitudinal shortening (%S: sonomicrometry) of both the anterior and posterior papillary muscles (PPM) were measured. MR was assessed by left ventricular contrast two-dimensional echocardiography. In eight dogs, all the data were adequate for analysis. In category 3 (C3: 55-70% CBF of control), %S in PPM decreased, but %W did not change significantly, and only mild MR developed in three of the eight dogs. MR clearly developed in category 4 (C4: 40-54% CBF as compared with the control stage), where %S was replaced by holosystolic lengthening and %W reduced to 50% of the control state, and total occlusion (C6) accompanied by significant thinning of both the PW and AW. Thus, the asynergy of the LVPW was needed to induce the MR in seven of the eight dogs. It was concluded that the injury of the PPM alone is not sufficient to cause MR, and the associated ischemic changes of the LV free wall as well as LV dilatation are necessary to induce severe MR.

Animals↗

PubMed1988

The circulating alpha 1-antitrypsin-elastase complex attacks the elastic lamina of blood vessels. An immunohistochemical study.

The aim of the study was to determine the destination of the alpha 1-antitrypsin-elastase complex, which is found in circulating blood after the peroral administration of elastase. The complex was made in vitro by mixing hog pancreatic elastase with human alpha 1-antitrypsin and then injected intravenously into rats and mice. Tissues taken at various times after injection were subjected to histochemical staining using an antibody against elastase. Light microscope observations revealed dense deposition of reaction products in the elastic lamina of the arterioles; moderate or slight deposits were seen in the tissues surrounding arteries, in the tubular epithelial cells of the proximal convoluted tubules in the kidney, and in the pancreatic ducts. Immunoelectron microscopy revealed heavy deposition of the reaction product in the elastic lamina of the small arteries and arterioles; some dissolution of the elastic fibers was also evident. Pinocytic uptake of the alpha 1-antitrypsin-elastase complex was observed on the abluminal surface of endothelial cells and in smooth-muscle cells bordering the elastic lamina of arterioles. The endothelial cells of the arteries and arterioles retained their normal morphological appearance, although local desquamation was observed in some animals. The results indicate that, when the alpha 1-antitrypsin-elastase complex is present in the circulating blood, it is incorporated into the elastic lamina through the endothelial layer. This results in liquefaction of the lamina, desquamation of endothelial cells and leakage of the complex into the perivascular tissues via the vascular walls. However, some of the complex seems to be excreted very quickly from the kidneys.

Animals↗

PubMed1988

Application of adjuvant-induced local hyperthermia for evaluation of anti-inflammatory drugs.

A recently established method for determining the surface temperature of adjuvant-inflamed rat's paw was used to examine the anti-inflammatory potencies of various nonsteroidal and steroidal anti-inflammatory drugs, which are currently in clinical use. The results were compared with those obtained by the carrageenin paw edema method and with the inhibitory potencies on prostaglandin E2 generation. The clinically effective single doses of the drugs were better correlated with the effective doses on local hyperthermia than with those on carrageenin paw edema, or with the inhibitory activities of the drugs on prostaglandin E2 generation from cultured rat synovial cells. Although care should be taken to avoid false-positive anti-inflammatory effects arising from vasoconstrictor activity or toxicity, determination of lowering effects on local hyperthermia in this inflammatory model may be useful for the evaluation of anti-inflammatory compounds.

Animals↗

PubMed1988

[Analysis of digital subtraction angiography for estimating flow reserve in critical coronary artery stenosis].

To assess the accuracy of digital subtraction angiography in evaluating coronary flow reserve in cases with critical coronary artery stenosis, time-density curves were obtained from digital subtraction coronary angiograms in the myocardial region of interest. Time to peak contrast (TPC) and time constant of the washout exponential curve (T) were measured in 14 patients with stable effort angina pectoris and critical one vessel lesion before and after percutaneous transluminal coronary angioplasty (PTCA). All patients had normal left ventricular ejection fraction (59 +/- 7%) and 201T1 myocardial images at rest. The values of TPC and T were significantly shortened from 5.4 +/- 1.3 to 4.5 +/- 1.0 sec (p less than 0.02) and from 10.9 +/- 3.8 to 5.3 +/- 1.3 sec (p less than 0.001) after PTCA, respectively. However, in 9 patients TPC values were approximately the same before and after PTCA. In five experimental dogs with critical circumflex coronary artery stenosis, coronary flow (CF; Doppler flowmeter) and systolic thickening of the posterior wall (by sonomicrometry) at rest did not differ from those of the controls. However, contrast media-induced reactive hyperemia was markedly attenuated, accompanied by a significant increase in T (7.7 +/- 4.5 vs 15.8 +/- 10.9 sec, p less than 0.01) and totally unchanged TPC (both 6.8 sec). With simultaneous tracings of CF and time-density curves, TPC and washout phases corresponded with contrast-induced transient CF reduction and hyperemic phases, respectively. We concluded that T may be more sensitive for estimating CF maintained nearly normal, e.g., in patients with stable effort angina pectoris having normal left ventricular wall motion at rest.

Aged↗

PubMed1988

Hepatic circulation and hepatic oxygen consumption in alcoholic and nonalcoholic fatty liver.

The purpose of this study was to determine the differences in hepatic circulation and oxygen consumption in two groups: those with nonalcoholic obesity-related fatty live and those with alcoholic fatty liver. Although the histological degree of fatty infiltration was equal in the two groups, the delta Er569-650, as an index of the regional liver blood flow estimated by spectrophotometric method, was significantly lower in alcoholic fatty liver than in nonalcoholic fatty liver, and the in vivo hepatic oxygen consumption (VO2), also determined by hepatic reflectance spectrophotometry during peritoneoscopy, tended to be lower in alcoholic fatty liver than in nonalcoholic fatty liver. The oxygen saturation of hemoglobin in local liver blood (SO2) was, however, significantly higher in alcoholic fatty liver than in nonalcoholic fatty liver. These results suggest that an increase in oxygen extraction to maintain oxygen consumption, which was indicated by the lowering of the SO2, was not found in alcoholic fatty liver, in spite of a reduction of oxygen supply to the liver. It is concluded that the impairment of hepatic circulation and hepatic oxygen consumption was more serious in alcoholic fatty liver than in nonalcoholic fatty liver, possibly contributing to a different prognosis for the two forms of fatty liver.

Fatty Liver, Alcoholic↗

PubMed1987

Time course of dolichol and dolichyl phosphate during chemical carcinogenesis in rat liver.

Hyperplastic liver nodules were induced in rats by administration of an initiator (diethylnitrosamine or 3'-methyl-4-dimethylaminoazobenzene) and/or a promoter (phenobarbital) by the method reported by Tatematsu et al. (1983, Carcinogenesis 4, 381-386). The dolichol content in the liver and liver microsomes of the rats treated with the initiator were approx. 1.5-times higher than that of the control and rats treated with only the promoter. However, the composition of dolichols was not changed. The time course of the dolichyl phosphate concentration in the rat liver treated with both initiator and promoter showed a pattern different from that in the control liver, the initiator-treated liver or the promoter-treated liver. The main component of dolichyl phosphate in liver treated with both the initiator and promoter changed from that with 18 isoprene units to that with 19. It is suggested that the changes in liver dolichols and dolichyl phosphates may be related to the formation of hyperplastic liver nodules.

Acyl Coenzyme A↗

PubMed1987

Pharmacological properties of N-methoxy-3-(3,5-ditert-butyl-4-hydroxybenzylidene)-2-pyrrolidone (E-5110), a novel nonsteroidal antiinflammatory agent.

The antiinflammatory activity of a novel pyrrolidone derivative E-5110 was investigated using anti-inflammatory, analgesic and antipyretic animal models in comparison to indomethacin (IND) and piroxicam (PIR). The acute antiinflammatory activity of E-5110 on carrageenin paw edema was similar to IND, and half of PIR. E-5110 inhibited the pleural exudate volume and leucocyte infiltration in a reversed passive Arthus reaction more potent than IND. The chronic inflammatory responses in the established adjuvant- and type II collagen-induced arthritis were suppressed by E-5110 similar to IND and PIR. The analgesic potency of E-5110 was similar to IND and PIR, but the antipyretic activity of E-5110 was more potent than that of IND, and slightly more potent than that of PIR. The ulcerogenic effect of E-5110 on rat gastric mucosa was less than that of the reference drugs.

Animals↗

PubMed1987

In vitro effect of N-methoxy-3-(3,5-ditert-butyl-4-hydroxybenzylidene)-2-pyrrolidon e (E-5110), a novel nonsteroidal antiinflammatory agent, on generation of some inflammatory mediators.

Cultured rat synovial cells generate PGE2 upon stimulation with a factor derived from rate polymorphonuclear cells (Prostaglandins 27, 697, 1984). E-5110 inhibited PGE2 generation by the synovial cells. The IC50 values (microM) for inhibition of PGE2 generation were 0.026 for E-5110, 0.008 for indomethacin, 0.112 for piroxicam, 0.003 for R-830, 0.667 for BW-755C and 2.05 for benoxaprofen. Calcium ionophore A-23187-stimulated LTB4 generation by human neutrophils was inhibited by E-5110 with an IC50 value of 0.20 microM, which was similar to NDGA. The inhibition of LTB4 by E-5110 was more potent than that of R-830, BW-755C or benoxaprofen. E-5110 also inhibited superoxide generation by human neutrophils stimulated with opsonized zymosan, f-Met-Leu-Phe and phorbol myristate acetate. These results indicate that E-5110 is a potent dual inhibitor that suppresses superoxide generation.

Animals↗

PubMed1987

Synthesis and antiinflammatory activities of 3-(3,5-di-tert-butyl-4-hydroxybenzylidene)pyrrolidin-2-ones.

A series of 3-(3,5-di-tert-butyl-4-hydroxybenzylidene)pyrrolidin-2-ones was synthesized and evaluated as candidate antiinflammatory/analgesic agents as well as dual inhibitors of prostaglandin and leukotriene synthesis. Some compounds that showed dual inhibitory activity were found to possess equipotent antiinflammatory activities to indomethacin, with reduced ulcerogenic effects. One of the compounds, N-methoxy-3-(3,5-di-tert-butyl-4-hydroxybenzylidene)pyrrolidin-2-o ne, was found to have a wider safety margin than indomethacin or piroxicam, and was selected for detailed evaluation as a candidate drug for clinical application.

Animals↗

PubMed1987

Evaluation of aortic wall distensibility by aortic pressure-dimension relation: effects of nifedipine on aortic wall.

The relation between aortic pressure and dimension was studied before and after nifedipine infusion in eight anaesthetised dogs. An electromagnetic flowmeter was positioned in the proximal ascending aorta and one pair of ultrasonic dimension gauges attached to the thoracic aorta. A Millar micromanometer was positioned just below the dimension gauges. A constrictor was placed around the thoracic aorta distal to the dimension gauges to produce an abrupt rise in aortic pressure for 15 s. After complete recovery nifedipine (0.75 micrograms.kg-1.min-1) was infused for 10 min and the same procedure repeated. The ratio (delta D:delta P) of the difference (delta D) between maximum and minimum dimensions (D) to the pulse pressure (delta P) and the percentage distensibility (delta D/delta P/minimum D) were decreased significantly after aortic constriction (0.037(0.013) to 0.019(0.004) mm.mmHg-1 and 0.247(0.075) to 0.121(0.033)%.mmHg-1, p less than 0.01, respectively), suggesting that these indices depend on afterload. Beat to beat mean pressure-dimension relations during the release of aortic constriction showed a convex upward curve and was fitted by an exponential function with a high correlation coefficient (r = 0.99). The slope of this relation was significantly reduced after nifedipine compared with before nifedipine (379(83) to 330(119) mmHg.cm-1, p less than 0.05), suggesting an increase in aortic distensibility by nifedipine. When mean aortic pressure or stroke volume before and after nifedipine was compared at the same mean dimension, which was reduced by 5% of the control mean dimension, stroke volume increased to 128%(p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗

PubMed1987

Effect of azelastine on the release and action of leukotriene C4 and D4.

The effect of azelastine on the release of leukotriene C4 and D4 (LTC4 and LTD4), and the antagonistic action of the drug against the leukotrienes were determined by using in vitro tests and compared with those of ketotifen and chlorpheniramine. Azelastine inhibited LTC4 and LTD4 release from guinea pig lung fragments passively sensitized with homologous anti-ovalbumin IgGl-b antibody. The 50% inhibitory concentration (IC50) of azelastine was 6.4 X 10(-5) M for a 15-min preincubation or 4.7 X 10(-5) M for a 30-min preincubation. Ketotifen and chlorpheniramine were inhibitory only at the highest concentration tested (3 X 10(-4) M), giving inhibitions of 35.6 and 21.3%, respectively. Azelastine also inhibited calcium ionophore A23187-induced release of leukotrienes from human polymorphonuclear leukocytes; the IC50 values were 3.6 X 10(-5) M for 15 min and 2.3 X 10(-6) M for 30 min of preincubation. Ketotifen and chlorpheniramine were inhibitory only after a 30-min preincubation, with IC50 values of 2.1 X 10(-5) and 5.9 X 10(-5) M, respectively. The potent inhibition by azelastine might be partly a result of the inhibition of 5-lipoxygenase, since 5-hydroxyeicosatetraenoic acid formation in rat basophilic leukemia cell homogenate was inhibited by azelastine. Pretreatment of guinea pig ileum with azelastine antagonized LTC4- and LTD4-induced contraction of the ileum with IC50 values of 7.0 X 10(-6) and 1.1 X 10(-5) M, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1987

Pharmacokinetic and pharmacodynamic studies of piretanide in rabbits. I. Effect of different hydrated conditions.

The pharmacokinetics and pharmacodynamics of piretanide in rabbits were investigated. After intravenous administration, the plasma concentrations and the urinary excretion rates of piretanide, as well as the pharmacologic effects, were measured under two different hydrated conditions. In one experiment, the amount of the body fluid which was lost during diuresis was replaced by infusing Ringer's solution at exactly the same rate with the urine flow rate (treatment I). In another experiment, no compensatory infusion was made (treatment II). There was no appreciable difference between treatment I and II, as far as the plasma concentrations and urinary excretion rate were concerned. In spite of the similarities in the pharmacokinetic properties, the pharmacologic effects of piretanide were influenced considerably by the hydrated conditions of the body. The diuretic effect expressed as the excretion rate of the sum of urinary sodium and potassium was plotted against the corresponding urinary excretion rate of unchanged piretanide. The shape of the each graph showed a similar sigmoid like curve; however, the curve in treatment I was significantly shifted to the right compared to that in treatment II. This fact indicated that the pharmacologic effect of piretanide seemed to be modified by the contents of water and electrolytes in the body. The plasma concentrations and urinary excretion of piretanide were reasonably described by a linear three compartment open model.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1987

Studies on the monoexponential nature of the left ventricular pressure fall during isovolumic relaxation period in the diseased heart.

Our recent clinical studies on the negative dP/dt upstroke pattern suggested that the left ventricular pressure (LVP) deviated from the exponential curve during isovolumic relaxation period (IRP) in diseased hearts. To examine this further two types of monoexponential curve fitting were done in various heart diseases (normal (N): 8, angina pectoris (AP): 8, myocardial infarction (MI): 13, hypertrophic cardiomyopathy (HCM): 10, dilated cardiomyopathy (DCM): 8). LVP was measured by a Millar's catheter-tip transducer, and four types of time constant (T1-T4) were derived: T1 was calculated by an exponential curve fitting e-t/T1 + B (B is constant), T2 by the ratio Pm/peak (-) dP/dt (Pm is LVP at peak (-) dP/dt), T3 by the best exponential curve fit e-t/T3 + B + C (C is constant), and T4 by the ratio (Pm-C)/peak (-) dP/dt. If the exponential curve fitting was reasonable, the relation between T1 and T2, or T3 and T4, should be on the line of identity. The result was as follows: T2 = 1.4 T1 - 6.1 (r = 0.84) and T4 = 1.1 T3 - 10.7 (r = 0.94). Additionally, C (mmHg) in MI (-26 +/- 15), HCM (-36 +/- 19) and DCM (-32 +/- 20) were lower (p less than 0.05) than in N (-13 +/- 7). These findings suggest that the LVP during IRP could deviate from the monoexponential curve and that careful attention should be given to calculate the time constant in diseased hearts.

Adult↗

PubMed1987

Focal fatty change of the liver adjacent to the falciform ligament: CT and sonographic findings in five surgically confirmed cases.

Five cases of surgically confirmed focal fatty infiltration of the liver were detected by CT and sonography. In all five cases, the abnormality was located at the anterolateral edge of the medial segment of the liver. It was seen as a small area of low attenuation adjacent to the falciform ligament on CT and as an echogenic area next to the ligamentum teres on sonography. Dynamic CT performed during infusion of contrast medium via the superior mesenteric artery (arterial portography) showed portal blood flow within the lesion and was useful for excluding the presence of a hepatic tumor. Focal fatty infiltration of the liver adjacent to the falciform ligament constitutes a diagnostic pitfall on CT and sonography.

Fatty Liver↗