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Biomedical subjects

J Azuma

Publications and source records attributed to J Azuma.

At least 55 records · Page 3Linked to original sources
PubMed1997

Renal excretory responses to saline load in the taurine-depleted and the taurine-supplemented rat.

Taurine is found in high concentrations in mammalian cells. Despite recognition of its role as an organic osmolyte in the kidney, information regarding its effects on renal fluid and electrolyte excretion is sparse. Therefore, the objective of the first series of experiments was to determine the effects of taurine depletion on renal excretory responses to a saline load. To induce taurine depletion, male Wistar-Kyoto (WKY) rats were treated with tap water containing 3% beta-alanine for 3 weeks. Taurine depletion reduced the initial rates of fluid and sodium excretion after an intravenous saline load. This effect was attributed to taurine depletion since maintenance of the taurine-depleted rats on tap water for 2 days to remove the effects of beta-alanine yielded the same pattern as the taurine-depleted rats exposed to beta-alanine at the time of the experiment. Nonetheless, rats exposed to short-term beta-alanine treatment, which has no influence on kidney taurine content, demonstrated a larger (approximately 25%) natriuretic but not diuretic response to the isotonic saline load than either the control or taurine-depleted rats. These data suggest that beta-alanine-induced inhibition of tubular reabsorption of taurine may result in subsequent excretion of taurine with attendant natriuresis early in the course of beta-alanine treatment. We also tested the hypothesis that taurine potentiates the renal excretory responses to an isotonic saline load in WKY rats. Inclusion of taurine in the infusate significantly increased natriuresis and diuresis after a saline load. This effect was greater in animals fed a basal than a high NaCl diet. Our data support a role for taurine as a natriuretic and diuretic agent.

Animals↗
PubMed1997

Effect of taurine on angiotensin II-induced hypertrophy of neonatal rat cardiac cells.

The effect of taurine on angiotensin II-induced hypertrophy of cultured neonatal rat heart cells (myocytes and nonmyocytes) was examined. Angiotensin II (1-100 nM) alone caused an increase in the rate of protein synthesis of myocytes without changing the rate of DNA synthesis and cell number. It mediated increases in DNA synthesis and cell number in nonmyocytes. Furthermore, at the lower concentration of 1 nM, it induced c-fos and c-jun expression in both cultured myocytes and nonmyocytes. Exposure of the cells to taurine (20 mM) in the absence of angiotensin II had no effect on either hyperplastic growth or immediate early response gene expression by the two types of cultured cardiac cells. However, myocytes pretreated for 24 h with 20 mM taurine exhibited reduced responsiveness to angiotensin II (1 nM), resulting in lower levels of angiotensin II-mediated stimulation in protein synthesis, and immediate early response gene expression was attenuated. Similarly, taurine treatment of nonmyocytes reduced the degree of hyperplastic growth (DNA synthesis and cell number) and immediate early response gene expression stimulated by angiotensin II. Finally, taurine partially prevented the increase in intracellular free calcium [Ca2+]i mediated by angiotensin II in cardiac cells. Our results indicate that taurine is an effective inhibitor of angiotensin II action.

Angiotensin II↗
PubMed1996

Protective effect of taurine against reperfusion injury in cultured rat astrocytes.

Reperfusion of cultured rat astrocytes with Ca(2+)-containing medium after exposure to Ca(2+)-free medium for a short time caused an increase in intracellular Ca2+ ([Ca2+]i), and delayed cell death (Ca2+ paradox-like injury). Exposure of astrocytes to Ca(2+)-free medium caused a marked release of taurine. Taurine (3-30 mM) reduced the reperfusion-induced increase in [Ca2+]i and attenuated the delayed glial cell death. Glycine, GABA and beta-alanine did not affect reperfusion-induced cell toxicity. The protective effect of taurine required addition at an early time during reperfusion. Ouabain and monensin mimicked reperfusion injury and their toxicity was also reduced by taurine. Taurine (3-30 mM) inhibited dose-dependently 45Ca2+ uptake stimulated by ouabain and monensin in astrocytes. These findings suggest that taurine has a protective effect against reperfusion injury via an inhibition of Na+/Ca2+ exchange activity in the reverse mode.

Animals↗
PubMed1996

Temporal changes in regional end-diastolic wall thickness early after reperfusion in acute anterior myocardial infarction: relation to myocardial viability and vascular damage.

We investigated early temporal changes in end-diastolic wall thickness (EDWT) of the infarcted myocardium in 46 patients with reperfused anterior acute myocardial infarction in relation to myocardial viability. Two-dimensional echocardiography was performed on days 1 and 2 of acute myocardial infarction, and the EDWT of the anterior segment was measured in the short-axis view. Patients were divided into three groups on the basis of day 1 to day 2 ratio of EDWT: the ratio < or = 0.85 as group A (n = 13), >0.85 but < or = 1.15 as group B (n = 23), and >1.15 as group C (n = 1 0). Left ventricular functional improvement was significantly better in group B than in groups A and C. Substantial size of "no reflow" phenomenon was observed only in groups A (n = 9, 69%) and C (n = 6, 60%). The frequency of transient ST re-elevation after reperfusion was the highest in group C (70%), and left ventricular expansion was observed at day 2 only in group A. We conclude that changes in the EDWT of the infarct segment early after reperfusion, either decreases or increases, are related to irreversibly damaged myocardium. A decrease in EDWT and concomitant ventricular expansion may be related to impaired myocardial perfusion. An increase in EDWT after reperfusion may be caused by accelerated myocardial and microvascular damage after reperfusion.

Adult↗
PubMed1996

Involvement of Na+-Ca2+ exchanger in reperfusion-induced delayed cell death of cultured rat astrocytes.

In some cells, Ca2+ depletion induces an increase in intracellular Ca2+ ([Ca2+]i) after reperfusion with Ca2+-containing solution, but the mechanism for the reperfusion injury is not fully elucidated. Using an antisense strategy we studied the role of the Na+-Ca2+ exchanger in reperfusion injury in cultured rat astrocytes. When astrocytes were perfused in Ca2+-free medium for 15-60 min, a persistent increase in [Ca2+]i was observed immediately after reperfusion with Ca2+-containing medium, and the number of surviving cells decreased 3-5 days later. The increase in [Ca2+]i was enhanced by low extracellular Na+ ([Na+]0) during reperfusion and blocked by the inhibitors of the Na+-Ca2+ exchanger amiloride and 3, 4-dichlorobenzamil, but not by the Ca2+ channel antagonists nifedipine, Ca2+ and Ni2+. Treatment of astrocytes with antisense, but not sense, oligodeoxynucleotide to the Na+-Ca2+ exchanger decreased Na+-Ca2+ exchanger protein level and exchange activity. The antisense oligomer attenuated reperfusion-induced increase in [Ca2+]i and cell toxicity. The Na+-Ca2+ exchange inhibitors 3, 4-dichlorobenzamil and ascorbic acid protected astrocytes from reperfusion injury partially, while the stimulators sodium nitroprusside and 8-bromo-cyclic GMP and low [Na+]0 exacerbated the injury. Pretreatment of astrocytes with ouabain and monensin caused similar delayed glial cell death. These findings suggest that Ca2+ entry via the Na+-Ca2+ exchanger plays an important role in reperfusion-induced delayed glial cell death.

Amiloride↗
PubMed1996

Ca2+ depletion facilitates taurine release in cultured rat astrocytes.

Removal of external Ca2+ facilitated endogenous taurine release in cultured rat astrocytes. The stimulated release was not affected by furosemide, sucrose, tetrodotoxin and 3,4-dichlorobenzamil, but partially inhibited by nifedipine. Omission of external Na+ increased basal taurine release, and the effects of Na+ removal and Ca2+ depletion on the release were additive. The Na(+)-free condition did not affect Ca2+ paradox-induced cell death in astrocytes. These findings suggest that Ca2+ depletion facilitates taurine release in a mechanism independent of volume and the Na+ gradient and that the release is not involved in Ca2+ paradox-induced delayed cell toxicity in astrocytes.

Amiloride↗
PubMed1995

Hypoxic stress induces cardiac myocyte-derived interleukin-6.

BACKGROUND: Hypoxic and ischemic stresses cause a series of well-documented changes in myocardial cells and tissues, including loss of contractility, changes in lipid and fatty acid metabolism, and irreversible membrane damage leading to eventual cellular death. Activated neutrophils are considered to be involved in this myocardial cellular injury. By stimulation of the neutrophils with chemotactic factors, canine neutrophils can be induced to adhere to isolated cardiac myocytes only if the myocytes have been previously exposed to cytokines such as tumor necrosis factor-alpha, interleukin (IL)-1, and IL-6. METHODS AND RESULTS: To examine the possible involvement of IL-6 in ischemia-reperfusion injury, we used cultured rat neonatal cardiac myocytes to study the effects of hypoxic stress on the production of IL-6 by cardiac myocytes. Unstimulated cardiac myocytes (3 x 10(5) cells per dish) produced 320 pg IL-6 over 4 hours in vitro (ie, biological activity equal to 320 pg recombinant IL-6, as detected by bioassay using the MH-60.BSF2 cell line). The incubation of cardiac myocytes under hypoxic conditions for 4 hours induced significantly increased production of IL-6 compared with normoxic conditions (2.82 +/- 0.49 versus 1.64 +/- 0.18 U/mL, P < .05). Furthermore, reoxygenation for 2 hours after 2 hours of hypoxic stress significantly augmented the production of IL-6 by cardiac myocytes (4.34 +/- 0.52 U/mL, P < .05). These responses to hypoxia and reoxygenation were not observed in fibroblasts isolated from the same tissue. Although unstimulated cardiac myocytes lacked IL-6 mRNA expression detectable by Northern blot analysis, hypoxic stress induced the expression of IL-6 mRNA in the cardiac myocytes. Several pathophysiologically relevant factors also augmented IL-6 release from cultured cardiac myocytes, including IL-1 beta, ionomycin, and epinephrine. CONCLUSIONS: Cardiac myocytes respond to hypoxic stress to augment the production of IL-6, and the IL-6 derived from cardiac myocytes may play an important role in the progression of myocardial dysfunction observed in cardiac ischemia-reperfusion injury.

Animals↗
PubMed1995

A missense mutation in the beta-myosin heavy chain gene in a Japanese patient with hypertrophic cardiomyopathy.

A 55-year-old man had been previously admitted at the age of 44 because of chest pain on effort. He was diagnosed as hypertrophic obstructive cardiomyopathy with a left ventricular outflow pressure gradient of 65 mmHg. We analyzed the cardiac beta-myosin heavy chain gene in this patient using polymerase chain reaction-single strand conformation polymorphism analysis (PCR-SSCP analysis). PCR-SSCP analysis revealed a sequence variation within exon 16. A G-to-A transversion with replacement of Val by Met at codon 606 was confirmed by sequencing analysis. Previously, a 606Val-->Met mutation has been reported to give a benign prognosis because of the neutral charge substitution. However, there have been some premature deaths in this patient's kindred. Thus, despite the absence of a change in charge, this mutation may be malignant in some kindreds.

Cardiomyopathy, Hypertrophic↗
PubMed1994

Prognosis of patients with severe congestive heart failure referred to the cardiac transplant program. Osaka University Cardiac Transplant Program.

In any program for cardiac transplantation, appropriate recipient selection is critically important. The purpose of this study is to evaluate the prognosis of 42 patients with severe cardiac dysfunction who were referred to the Patient Referral Committee of the Osaka University Cardiac Transplant Program from August 1990 to July 1993. All of the patient profiles and clinical data were presented and discussed in the Committee Conference. The Committee classified the patients into three groups according to the following criteria: Class A; 14 patients judged to have a medical indication for heart transplantation, Class B; 7 patients with possible indications which required reevaluation for a definite indication after further intensive medical treatments, and Class C; 21 patients who did not have indications for heart transplantation or who required further clinical examinations and/or medical treatments before a final judgment. Twelve of the 14 Class A patients had a history of NYHA functional class IV and ejection fractions were 25% or less in all of the patients but one (18.5 +/- 1.7%). Six patients in Class A had a history of ventricular tachycardia. The one-year survival rate of Class A patients was 60%, and only 28% survived for 28 months. One patient underwent successful heart transplantation in the United States. If we assume that this patient would have died within a year without heart transplantation, the estimated one-year survival rate would fall to 48%, which is comparable to the survival rate of patients who have been accepted for transplant, but are being treated medically, in Western countries.(ABSTRACT TRUNCATED AT 250 WORDS)

Actuarial Analysis↗
PubMed1994

Effect of taurine and methionine on sarcoplasmic reticular Ca2+ transport and phospholipid methyltransferase activity.

Perfusion of rat hearts with buffer containing 300 microM L-methionine led to a decrease in Ca(2+)-induced Ca2+ release in sarcoplasmic reticulum (SR) but an increase in calcium-independent Ca2+ release from junctional SR. These effects of L-methionine were not altered by exposure of the hearts to high levels of extracellular taurine, but changes in the size of the intracellular taurine pool appear to modulate calcium transport in SR through two mechanisms. First, millimolar concentrations of taurine can directly promote release of calcium from 45Ca(2+)-loaded junctional SR vesicles. Second, taurine serves as an inhibitor of SR phospholipid methyltransferase, an enzyme that appears to be responsible for methionine-mediated loss in Ca(2+)-induced Ca2+ release activity and promotion of Ca(2+)-independent Ca2+ release. The data imply that modulation of the intracellular taurine pool may affect cellular calcium homeostasis and myocardial contractile function. This may be important in development of the cardiomyopathy linked to taurine deficiency.

Animals↗
PubMed1994

[Metabolic and endocrinological responses to the infusion of a new intraoperative fluid].

A new intraoperative fluid, which is characterized by containing 10 mEq.l-1 of potassium, 140 mEq.l-1 sodium and 1% glucose, was infused into 18 healthy volunteers either at rate of 5, 10 ml.kg-1.h-1 (for 3 hours) or 15 ml.kg-1.h-1 (for 2 hours). Responding to increase in the infusion rate and volume, blood glucose and insulin (IRI) levels increased slightly but remained in the normal range. On the other hand, lipid metabolism was depressed markedly. Although concentrations of both potassium and sodium in serum remained unchanged, sodium and water balance (intake vs. outflow) became absolutely positive. Potassium balance was maintained at zero. Blood renin activity decreased gradually after the infusion was commenced and remained at a lower level for 3 hours after stopping infusion. Blood aldosterone and antidiuretic hormone levels also decreased but more gradually than the decrease of blood renin activity. Noteworthy change was not observed in the variables relating to hepatic and renal functions.

Adult↗