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Biomedical subjects

Y Tsuruya

Publications and source records attributed to Y Tsuruya.

At least 19 recordsLinked to original sources
PubMed2004

Functional and anatomical effects of hormonally induced experimental prostate growth: a urodynamic model of benign prostatic hyperplasia (BPH) in the beagle.

BACKGROUND: Benign prostatic hypertrophy (BPH) produces a variety of changes in the urodynamic pattern of micturition and is usually associated with high detrusor voiding pressure and poor urine flow-rate. In most previous experimental models, designed to simulate this condition, some degree of obstruction is immediately imposed by the technique employed to produce urethral occlusion. Consequently these models cannot reproduce the gradual onset of obstruction. In the present study a canine prostatic enlargement model, using 5alpha-dihydrotestosterone (DHT) + 17beta-estradiol (E) was adapted in order to produce a more gradual onset of partial obstruction and impaired voiding. MATERIALS AND METHODS: Hormonally induced prostatic enlargement was produced using seven beagles, given DHT 75 mg/day together with E 0.75 mg/day for 28 days via an implantable pump. The functional effects of DHT + E treatment on micturition pressure/flow were measured in the conscious animal. Identical measurements were also made using a separate older group of five beagles with symptoms of BPH. In addition seven beagles similarly instrumented were used as controls. RESULTS: Pressure/flow studies show that DHT + E produced obstructive micturition, characterized by a significantly increased micturition detrusor pressure, from 33.3 +/- 10.5 to 50.8 +/- 10.7 cmH(2)O and significantly decreased low urine flow-rate from 8.6 +/- 2.1 to 6.9 +/- 0.9 ml/sec. Associated with the obstructive micturition, this treatment increased wet prostate weight from 11.9 +/- 2.5 to 31.6 +/- 10.0 g. Prostate volume of the BPH beagles was 29.3 +/- 8.9 g. Morphologic studies show that DHT + E produced epithelial hyperplasia extending focally into the lumen. CONCLUSIONS: Hormonally induced prostate growth produced bladder obstruction, in terms of pressure/flow characteristics, that are analogous to BPH. It is suggested that this type of hormonal treatment can be used to create a model for the study of the effects of controlled increased in prostate growth and the development of BPH on micturition.

Age Factors↗
PubMed2004

Nicorandil versus isosorbide dinitrate as adjunctive treatment to direct balloon angioplasty in acute myocardial infarction.

OBJECTIVE: To compare the effects of nicorandil (a hybrid ATP sensitive potassium channel (K+(ATP) channel) opener/nitric oxide donor) with those of isosorbide dinitrate (ISDN) on myocardial microcirculation and cardiac function in patients with acute myocardial infarction (AMI) who had undergone reperfusion treatment by direct balloon angioplasty. DESIGN: Double blind randomised study. PATIENTS: 60 patients with AMI in Killip class I. INTERVENTIONS: Patients were assigned into two treatment groups: a nicorandil group (n = 30) and an ISDN group (n = 30). Each drug was infused intravenously at 6 mg/h for 72 hours starting at admission and was administered directly to the treated coronary artery immediately after angioplasty. RESULTS: Compared with ISDN, nicorandil more frequently caused recovery of ST segment elevation just after reperfusion (15 of 27 (55.5%) in the nicorandil group v 5 of 26 (19.2%) in the ISDN group, p = 0.006). The nicorandil group had higher values of averaged peak velocity 40 minutes after reperfusion (mean (SD) 24.8 (13.3) cm/s v 16.0 (11.1) cm/s, p = 0.045) and higher values of regional wall motion of the infarcted area three weeks after onset of AMI (-1.78 (1.11) v -2.50 (1.04) SD/chord, p = 0.046). CONCLUSIONS: A combination of nicorandil drip infusion starting before reperfusion and intracoronary injection immediately after reperfusion is more effective than a similarly performed infusion of ISDN in preserving myocardial microcirculation in the reperfused AMI area. The nicorandil regimen resulted in better left ventricular regional wall motion.

Angioplasty, Balloon↗
PubMed2001

[The voiding after the suburethral sling operation, obstructive or non-obstructive?].

To examine whether or not the suburethral sling operation produces obstruction during voiding, seven females who underwent the sling operation using synthetic material (Vesica Sling Kit) were studied postoperatively urodynamically. Uroflowmetry and residual urine measurement showed no overt voiding difficulties in any cases. However, in one case, a pressure flow study indicated equivocal and the position of the sling material was judged to be too proximal by fluoroscopic monitoring. In all other 6 cases pressure flow was shown to be non-obstructive. Fluoroscopic finding also demonstrated in these 6 cases an appropriate bladder neck opening at the time of voiding and the sling was positioned just from the bladder neck to mid-urethra. Thus, it is concluded that the suburethral sling operation produces no obstruction as long as the position of the sling material is carefully determined from bladder neck to mid-urethra and excessive tension is avoided.

Aged↗
PubMed2001

[Tubulointerstitial nephritis in the case of acute renal failure from sepsis after a cat bite].

Acute tubulointerstitial nephritis is associated with a variety of causes, such as drug interaction, and infectious or immunological mechanisms. We describe a patient who suffered from sepsis, septic shock, disseminated intravascular coagulation(DIC), hepatic failure and renal failure after receiving a bite from her house cat. The causes of her acute renal failure were initially thought to be due to circulatory failure with hypotensive shock, decrease in renal blood flow with fibrin formation by DIC, or microangiopathy such as hemolitic uremic syndrome. However, the renal biopsy on the 60th hospital day indicated tubulointerstitial nephritis, which was recognized by the presence of patchy and focal mononuclear small cell infiltration with invasion to the tubular epithelium. We concluded that prolonged renal failure was caused by tubulointerstitial nephritis. The cause of tubulointerstitial nephritis was not identified. Tubulointerstitial nephritis should be taken into consideration when the recovery from acute renal failure is slow.

Acute Kidney Injury↗
PubMed1998

[A case of neutropenic enterocolitis in high dose chemotherapy with peripheral blood stem cell transplantation for relapsed testicular tumor].

High dose chemotherapy with peripheral blood stem cell transplantation (PBSCT) is safe and useful for the treatment of refractory or relapsed testicular tumors, but is sometimes accompanied by serious complications. We report a case of relapsed testicular tumor complicated by neutropenic enterocolitis during high dose chemotherapy with PBSCT.

Adult↗
PubMed1997

Thyroid hormone stimulates Na(+)-Ca2+ exchanger expression in rat cardiac myocytes.

We investigated whether thyroid hormone directly affects Na(+)-Ca2+ exchanger expression in cardiac myocytes. Cultured neonatal rat cardiocytes were prepared from 1-day-old Sprague-Dawley rats. Intracellular Na+ concentration ([Na+]i) in cardiocytes was measured by using the Na(+)-sensitive dye sodium-binding benzofran isophthalate (SBFI). Na(+)-Ca2+ exchanger messenger RNA (mRNA) and protein expression were assayed by Northern and Western blotting, respectively. Triiodothyronine (T3; 10(-8) M) showed no effect on [Na+]i in cardiocytes, whereas ouabain (100 microM) caused a significant increase in [Na+]i from 11.3 +/- 5.0 to 21.8 +/- 5.0 mM. Exposure of cardiocytes to ouabain caused a rapid increase in Na(+)-Ca2+ exchanger mRNA accumulation, with a maximal twofold elevation at 12 h. The ouabain-induced Na(+)-Ca2+ exchanger mRNA accumulation was still observed in the Ca(2+)-free culture medium. On the other hand, exposure of cardiocytes to T3 induced a gradual increase in Na+ exchanger mRNA accumulation, with a maximal threefold increase at 24 h. Even in Na(+)-free medium, T3 still induced a twofold increase in Na(+)-Ca2+ exchanger mRNA accumulation in cardiocytes. Exposure of cardiocytes to T3 for 24-48 h also caused a marked increase in Na(+)-Ca2+ exchanger protein accumulation. In conclusion, thyroid hormone directly increases cardiac Na(+)-Ca2+ exchanger expression, independent of alterations in Na+ mobilization. These findings suggest also that thyroid hormone and Na+ regulate Na(+)-Ca2+ exchanger gene expression through distinct molecular regulatory pathways.

Animals↗
PubMed1994

Molecular cloning and functional expression of the guinea pig cardiac Na(+)-Ca2+ exchanger.

The cDNA of the guinea pig cardiac Na(+)-Ca2+ exchanger was cloned from a lambda ZAP cDNA library. The deduced sequence of the protein corresponds to 970 amino acids and is 98% identical to the canine cardiac exchanger. The leader peptide region shows substantial variation among species. The cloned cDNA can induce Na(+)-Ca2+ exchange activity when in vitro transcribed cRNA is injected into Xenopus laevis oocytes.

Amino Acid Sequence↗
PubMed1994

Noninvasive evaluation of the influence of aortic wave reflection on left ventricular ejection during auxotonic contraction.

To develop a noninvasive method for evaluating the influence of aortic wave reflection on left ventricular ejection, the carotid pulse wave and the pulsed Doppler wave in the left ventricular outflow tract were evaluated in 35 patients. Agreement between the pulsed Doppler waveform and the aortic flow velocity contour (obtained invasively) was verified by Fourier analysis. The carotid augmentation index was used to determine the magnitude of the aortic pressure wave reflection. A Doppler index named "DR1/3" was defined as the ratio of deceleration at the first one-third in the deceleration phase to the peak flow velocity of the pulsed Doppler. This index was validated by close correlation with the carotid augmentation index (n = 48, r = 0.70, P < 0.01). Both nitrates and nifedipine induced a significant decrease in DR1/3 (indicating an increase in left ventricular ejection flow) in relation to a reduction of the reflected pressure wave. The new noninvasive index, DR1/3, is useful in evaluating the influence of aortic wave reflection as part of the left ventricular afterload and in assessing the benefit of treatment aimed at reducing wave reflection.

Aorta↗
PubMed1994

Decreased Na,K-ATPase gene expression in cardiomyopathic hamster hearts.

We studied Na,K-ATPase mRNA expression in cardiomyopathic (Bio 14.6) and normal (F1b) Syrian hamster ventricles. In Northern blot analysis, Na,K-ATPase alpha 1, alpha 2, alpha 3 and beta 1 isoform mRNAs were detected in 3-week-old Bio 14.6 and F1b hamster ventricles. We then investigated the expression of alpha 1 subunit mRNA in Bio 14.6 hamster ventricles at the ages of 3 weeks prehypertrophic and 30 weeks hypertrophic, and in age-matched F1b hamster ventricles. The alpha 1 subunit mRNA levels in Bio 14.6 hamster ventricles were approximately 50% lower than those in F1b hamster ventricles at both 3 and 30 weeks of age. Na,K-ATPase activity measured in membrane fractions from the ventricles of 3-week-old Bio 14.6 hamsters was also approximately 20% lower than that of F1b hamsters, suggesting that the differences in the mRNA level were associated with the differences in the protein level. We conclude that Na,K-ATPase mRNA expression and enzyme activity are significantly decreased in the hearts of Bio 14.6 hamsters even before the onset of hypertrophy and cardiomyopathy, suggesting that the altered expression of Na,K-ATPase gene is an early event in the pathogenesis of cardiomyopathy in this animal model.

Animals↗
PubMed1994

Altered levels of erythrocyte calcium-binding proteins in essential hypertensives with genetic predisposition: correlation with ambulatory blood pressure.

OBJECTIVE: To examine whether changes in calcium-binding proteins, one of the components of the calcium ion handling mechanism, occur in humans with essential hypertension. DESIGN: We measured the levels of cytosolic calcium-binding proteins purified from human erythrocytes using a felodipine fluorescence assay, and examined the correlation between this parameter and the ambulatory blood pressure (ABP). We divided 127 subjects into four age-matched groups according to their mean ABP levels and whether they had a family history of both hypertension and stroke [group A hypertensives with a positive family history (n = 30), group B hypertensives with no family history (n = 31), group C normotensives with a family history (n = 31) and group D normotensives with no family history (n = 35) of hypertension and stroke]. RESULTS: The erythrocyte cytosolic level of calcium-binding proteins in group A was significantly lower than that in group B, as was that in group C compared with group D. There was no significant correlation between the erythrocyte level of calcium-binding proteins and casual blood pressure values in any group. However, in group A significant negative correlations between the erythrocyte level of calcium-binding proteins and systolic and mean ABP were observed (r = -0.34, P < 0.05 and r = -0.39, P < 0.05, respectively). No significant correlations between the ABP and erythrocyte levels of calcium-binding proteins were observed in the other groups. When each group was subdivided according to sex, there were significant negative correlations between the erythrocyte level of calcium-binding proteins and the systolic and mean ABP in the males of groups A and C, but no correlations were found in any of the female subgroups or the males of groups B and D. Reducing the blood pressure by antihypertensive drug therapy did not affect the erythrocyte calcium-binding proteins level in 13 patients from groups A and B. Analysis using anion-exchange fast-performance liquid chromatography on a Mono-Q column and sodium dodecyl sulphate-polyacrylamide gel electrophoresis revealed that the calcium-binding proteins in human erythrocytes, the levels of which were low in group A, formed a single protein band with a molecular weight of 17,000, which was assumed to be a calmodulin. CONCLUSIONS: These results suggest that there are subgroups of hypertensive patients with low erythrocyte cytosolic levels of calcium-binding proteins, which are genetically determined. Furthermore, our data suggest that the erythrocyte level of calcium-binding proteins and ABP in male subjects with hypertension and normotensives with a genetic predisposition are correlated strongly, whereas no such correlation was observed in any female subgroup. This indicates that the regulatory mechanism or mechanisms involved in the control of blood pressure in men and women may be different.

Aging↗
PubMed1993

Alterations in cytosolic calcium-binding proteins that increase felodipine fluorescence in spontaneously hypertensive rats.

OBJECTIVE: To clarify the role of calcium-binding proteins (CaBP) in hypertension. DESIGN: CaBP from several organs of spontaneously hypertensive rats (SHR) and age-matched Wistar-Kyoto (WKY) rats were purified and their characteristics compared between the two strains. The CaBP were purified by applying the soluble cytosolic fractions from mesenteric vessels, heart, kidney and brain of 4- and 10-week-old SHR and WKY rats to a phenyl-Sepharose column. Felodipine binding to the purified CaBP was then measured. RESULTS: The fluorescence intensity of felodipine increased in a calcium-dependent manner when it bound to CaBP. The pK 0.5 Ca2+ values derived from the calcium ion-felodipine fluorescence curves for each CaBP preparation from organs of the two strains were similar, indicating that the calcium sensitivities of the CaBP to the felodipine binding process are similar in SHR and WKY rats. In 10-week-old SHR the mean levels of felodipine-bound CaBP in heart, brain and kidney were significantly altered compared with those in WKY rats. No such alterations were observed in heart, kidney and brain from 4-week-old SHR and WKY rats. Conversely, the mean levels of felodipine-bound CaBP in mesenteric vessels from 4- and 10-week-old SHR were reduced significantly compared with those of age-matched WKY rats. CONCLUSIONS: These results suggest that the levels of cytosolic felodipine-bound CaBP from heart, kidney and brain are altered in response to elevated blood pressure, and that reduced levels of felodipine-bound CaBP in the mesenteric vessels of SHR might be a primary characteristic of this rat strain.

Animals↗
PubMed1993

Regulation of Na-K-ATPase gene expression by aldosterone in vascular smooth muscle cells.

Na-K-adenosinetriphosphatase (ATPase) activity profoundly influences vascular cell excitability, contractility, and volume regulation. The recent finding of mineralocorticoid hormone receptors in vascular tissue suggests the possibility that Na-K-ATPase gene expression in vascular tissue is regulated by the mineralocorticoid aldosterone. In this study, we investigated Na-K-ATPase gene expression by aldosterone in cultured rat vascular smooth muscle cells (VSMC). Na-K-ATPase alpha 1- and beta 1-isoform mRNAs, but not alpha 2- and alpha 3-isoform mRNAs, were expressed in cultured rat VSMC. Aldosterone caused a 2.3-fold increase in the alpha 1 mRNA and a 4.7-fold increase in the beta 1 mRNA accumulation with peak elevations at 24 and 6 h, respectively. Aldosterone induced the alpha 1 mRNA expression at physiological concentrations (half-maximum effective concentration = 2-3 nM), consistent with the binding of aldosterone to mineralocorticoid hormone receptors. The augmented alpha 1 mRNA expression by aldosterone was associated with a twofold increase in the alpha 1-subunit protein accumulation. Pretreatment of VSMC with cycloheximide caused a 10-fold increase in the alpha 1 mRNA expression, and the aldosterone-mediated alpha 1 mRNA accumulation was not observed in the presence of cycloheximide. Transfection experiments with the luciferase reporter gene revealed that aldosterone response sequences are located within the 5'-flanking regions of the alpha 1-isoform gene. These data demonstrate that the mineralocorticoid aldosterone directly stimulates Na-K-ATPase gene expression and protein accumulation in VSMC.

Aldosterone↗
PubMed1993

Thyroid hormone stimulates Na(+)-K(+)-ATPase gene expression in cultured rat mesangial cells.

Thyroid hormone 3,3',5-triiodothyronine (T3) is an important regulator of Na(+)-K(+)-adenosinetriphosphatase (Na(+)-K(+)-ATPase) activity in a variety of mammalian target tissues. In the present study, we examined the expression of Na(+)-K(+)-ATPase alpha- and beta-subunit mRNAs by T3 in cultured rat mesangial cells. Northern blot analysis of total RNA isolated from cultured rat mesangial cells revealed the expression of mRNAs encoding Na(+)-K(+)-ATPase alpha 1- and beta 1-subunits; mRNAs encoding alpha 2- and alpha 3-subunits were undetectable. Exposure of mesangial cells to T3 (10(-8) M) caused a threefold increase in the alpha 1-mRNA expression, which was first detected at 6 h and sustained for at least 48 h. The beta 1-mRNA expression was gradually increased by T3, with a maximum fourfold elevation at 48 h. The 50% effective concentration (EC50) for the alpha 1- and beta 1-mRNA induction by T3 was approximately 10(-10) M. The half-life of alpha 1-mRNA analyzed by actinomycin D chase was approximately 3 h and was not affected by T3. The augmented alpha 1-mRNA expression by T3 was associated with a 2.4-fold increase in the alpha 1-subunit protein accumulation and a 1.6-fold increase in Na(+)-K(+)-ATPase activity. These data suggest that thyroid hormone stimulates Na(+)-K(+)-ATPase gene expression, protein accumulation, and enzyme activity in rat mesangial cells.

Animals↗
PubMed1993

Regulation of Na,K-adenosine triphosphatase gene expression by sodium ions in cultured neonatal rat cardiocytes.

Na,K-ATPase (Na,K-pump) plays an important role in the regulation of intracellular ion composition. The purpose of this study is to determine whether Na+ regulates the levels of mRNA coding for Na,K-ATPase alpha and beta subunits in cultured neonatal rat cardiocytes. We measured intracellular Na+ levels ([Na+]i) in cardiocytes using a Na(+)-sensitive fluorescence dye (SBFI). 1 mM ouabain caused a significant increase in [Na+]i in cardiocytes; from 12.8 +/- 0.3 to 28.8 +/- 1.8 mM. Exposure of cardiocytes to 1 mM ouabain resulted in a three- to fourfold increase in alpha 1, alpha 2, and alpha 3 mRNA accumulation, and an approximate two-fold increase in beta 1 mRNA accumulation. A maximum elevation was reached at 60 min in both cases. The ouabain-induced alpha 1 mRNA accumulation was still observed in the Ca(2+)-free culture medium. Exposure of cardiocytes to 10 microM monensin in the absence of extracellular Ca2+ also resulted in a threefold increase in alpha 1 mRNA accumulation. The increased alpha 1 mRNA expression by 1 mM ouabain was associated with a fourfold increase in alpha 1 subunit protein accumulation. Transfection experiments with chimeric plasmids containing 5'-flanking sequences of alpha 1, alpha 2, and alpha 3 isoform genes and a luciferase reporter gene revealed that 1 mM ouabain caused a twofold increase in luciferase activity in each alpha system. These results suggest that Na+ directly regulates Na,K-ATPase gene expression in cardiocytes. The transfection study further supports the premise that Na(+)-responsive elements are located within the 5'-flanking sequences of each alpha isoform gene.

Animals↗
PubMed1993

[Na, K-ATPase gene expression in hypertrophic and failing hearts].

Na, K-ATPase (Na, K-pump) maintains intracellular ion composition by transporting Na+ and K+ across the cell membrane, and plays an important role in many fundamental cellular and physiological processes such as the control of contractility, excitability, and cell volume regulation. The Na, K-ATPase protein comprises two subunits, a large catalytic alpha subunit and a smaller glycosylated beta subunit. At least three alpha subunit isoforms, alpha 1, alpha 2 and alpha 3, and two beta subunit isoforms, beta 1 and beta 2, have been characterized in rats and humans. The expression of Na, K-ATPase alpha and beta subunits in cardiocytes is directly regulated at a transcriptional level by hormones and ions, such as thyroid hormone and Na+. In the hypertrophic and failing hearts, the expression of cardiac Na, K-ATPase gene is altered, and which might play an important role in the pathogenesis of those disorders.

Animals↗
PubMed1992

Enhanced spontaneous calcium efflux and decrease of calcium-dependent calcium release from the isolated perfused heart of spontaneously hypertensive rats.

OBJECTIVE: The aim of this study was to clarify the further details of calcium handling in hypertension. DESIGN: By preserving the physiological environment of cell membrane, whole hearts were used for comparison of calcium flux between spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. METHODS: Hearts from SHR and WKY rats were perfused with Krebs-Henseleit solution under constant flow and the effluent collected. RESULTS: After labelling of the heart with 45Ca2+ (100 mumol/l), 45Ca2+ binding was found to be saturated, and washing with calcium-free perfusion solution showed two exponential curves for calcium dissociation, indicating a fast (alpha-) and slow (beta-) phase. The half-lives of the beta-phase for both 4- and 8-week-old SHR were significantly shorter than those for age-matched WKY. Also in this phase, infusion of non-radioactive Ca2+ caused a transient dose-dependent release of 45Ca2+. A significant reduction in the amount of 45Ca2+ release induced by 2 mmol/l Ca2+ was observed in both 4- and 8-week-old SHR compared with age-matched WKY rats. Infusion of lanthanum, caffeine, ionomycin (calcium ionophore) and treatment of the hearts with ethyleneglycol-bis-(beta-aminoethylether)-N,N,N,',N'-tetraac etic acid did not alter 45Ca2+ release by non-radioactive Ca2+. From these observations, 45Ca2+ is presumably released from the intracellular calcium pool, and not from extracellular binding sites or sarcoplasmic reticulum. CONCLUSIONS: These findings suggest that an abnormal calcium-handling defect (enhanced calcium efflux and reduction of membrane-bound Ca2+) exists under physiological conditions before and after the onset of hypertension, and that this may be a primary characteristic of SHR.

Aging↗
PubMed1992

Regulation of Na,K-ATPase gene expression by thyroid hormone in rat cardiocytes.

Synthesis and activity of the enzymatic equivalent of the sodium pump, Na,K-ATPase, are regulated by thyroid hormone in responsive tissues. The purpose of this study was to determine whether triiodothyronine (T3) regulates the level of the messenger RNA (mRNA) coding for Na,K-ATPase alpha- and beta-subunits in the heart. The expression of Na,K-ATPase mRNAs in in vitro myocardial cells was directly assayed by Northern and slot blot hybridization using Na,K-ATPase alpha- and beta-isoform-specific cDNA probes. Exposure of cultured neonatal rat cardiocytes to 10(-8) M T3 resulted in 1) threefold to fourfold increase in alpha 1- and beta 1-mRNA accumulation, with a maximum elevation at 48 hours, 2) sevenfold increase in alpha 2-mRNA accumulation with a peak elevation at 72 hours, and 3) transient threefold increase in alpha 3-mRNA within the first 24 hours followed by a deinduction thereafter. The increase in alpha 1-mRNA accumulation by T3 occurred over the physiological T3 concentration range with an EC50 of 5 x 10(-10) M. This was associated with a twofold increase in alpha 1-subunit protein accumulation and an increase in Na,K-ATPase transport activity. The half-life of alpha 1-mRNA analyzed by actinomycin D chase was less than 3 hours and was not affected by T3. Transfection experiments with the luciferase reporter gene revealed that thyroid hormone response sequences are located within the 5'-flanking regions of each alpha-isoform gene.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗