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H Arisaka

Publications and source records attributed to H Arisaka.

14 recordsLinked to original sources
PubMed2000

Clinical pharmacokinetics and effects of an oral sustained-release preparation of disopyramide prescribed for patients undergoing maintenance hemodialysis.

AIMS: We evaluated the clinical pharmacokinetics of a sustained-release preparation of disopyramide phosphate (DSR) and its effects on supraventricular arrhythmias in hemodialysis patients. METHODS: Eight hemodialysis patients with either paroxysmal supraventricular tachycardia (PSVT) or PSVT plus paroxysmal atrial fibrillation (Paf) were given 150 mg of DSR 2 h before each hemodialysis. The frequency of PSVT, the duration of Paf before and 2 weeks after starting DSR and the blood concentration of the drug were evaluated. RESULTS: There was no significant difference between serum levels of DSR before and after hemodialysis. The frequency of PSVT and the duration of Paf were significantly reduced by the therapy. Side effects and electrocardiographic abnormalities did not appear during the period. CONCLUSION: We conclude that hemodialysis does not remove DSR, and that a single dose of 150 mg of DSR given 2 h before hemodialysis is safe and sufficient to reduce the incidence of supraventricular arrhythmias.

Administration, Oral↗
PubMed2000

[Anesthetic management of patients with tracheal stenosis for endoscopic treatment: usefulness of laryngeal mask airway].

We report two cases of tracheal stenosis for endoscopic treatment under general anesthesia with laryngeal mask airway. The tracheal stenosis of the two patients was so close to the glottis that endotracheal tube could not be inserted, and laryngeal mask airway was beneficial for maintaining airway and obtaining operating field. During the procedure, patients breathed spontaneously and we could support their ventilation easily and sufficiently. Endoscopic treatment of the airway obstruction by Nd-YAG laser associated with balloon dilatation and stent is an effective method of relieving the distressing symptom of asphylaxia, and laryngeal mask airway is considered to be useful for performing successful endoscopic procedure.

Aged↗
PubMed1999

[The characteristics of myocardial fatty acid metabolism in patients with left ventricular hypertrophy].

We evaluated the characteristics of myocardial fatty acid metabolism in patients with left ventricular hypertrophy (LVH). Myocardial imaging with 123I-beta-methyl iodophenyl pentadecanoic acid (BMIPP) was performed in 28 patients with hypertrophic cardiomyopathy (HCM), 15 patients with hypertensive heart disease (HHD), 13 patients with aortic stenosis (AS) and 8 normal controls (NC). The patients with HCM consisted of 13 patients of asymmetric septal hypertrophy (ASH), 7 patients of diffuse hypertrophy (Diffuse-HCM) and 8 patients of apical hypertrophy (APH). Planar and SPECT images of BMIPP were acquired 15 minutes and 4 hours after tracer injection. Resting 201Tl SPECT images and echocardiography were also performed on other days. We calculated heart/mediastinum count ratio and washout rate of BMIPP by using planar image. In patients with LVH, the incidence of reduced BMIPP uptake was more frequent than that of reduced 201Tl uptake. In delayed images, more than 60% of patients with LVH reduced BMIPP uptake, especially remarkable for patients with ASH and APH. The washout rate of all cardiac hypertrophic disorders was tended to be higher than that of normal subjects. Reduced BMIPP uptake was frequently found in septal portion of anterior and inferior wall in patients with ASH, in inferior wall in patients with Diffuse-HCM and HHD, in apex in patients with APH and AS. These results suggest that BMIPP scintigraphy can differentiate three types of cardiac hypertrophy.

Aged↗
PubMed1997

Anti-thrombotic effects and bleeding risk of AJvW-2, a monoclonal antibody against human von Willebrand factor.

1. A murine anti-human vWF monoclonal antibody, AJvW-2, was developed that inhibited the interaction between platelet glycoprotein Ib (GPIb) and von Willebrand factor (vWF) during the ristocetin- (IC50 = 0.7 +/- 0.1 microgram ml-1) and botrocetin- (IC50 = 1.8 +/- 0.3 microgram ml-1) induced aggregation of human platelets. 2. AJvW-2 inhibited the high shear stress (10.8 N m-2) induced aggregation of human platelets dose-dependently with an IC50 = 2.4 +/- 0.3 micrograms ml-1, but had no effect on low shear stress induced platelet aggregation (1.2 N m-2) up to 100 micrograms ml-1. 3. AJvW-2 also inhibited the high shear stress (5.0 N m-2) induced adhesion of human platelets to collagen I with the same efficacy (IC50 = 2.4 +/- 0.3 micrograms ml-1), but no effect at low shear conditions (1.5 N m-2). 4. AJvW-2 inhibited the botrocetin-induced aggregation of platelets from guinea-pig, rat, rabbit, dog and pig at the same concentration range as human platelets; it likewise also inhibited the high shear stress induced aggregation and adhesion to collagen I of guinea-pig platelets. 5. AJvW-2 prevented arterial thrombus formation in guinea-pigs at a dose of 100 micrograms kg-1 without prolonging the template bleeding time, whereas the GPIIb/IIIa antagonists lamifiban mediated inhibition of thrombosis at 1000 micrograms kg-1 was accompanied by a significant prolongation of the bleeding time. 6. These results suggest that AJvW-2 is a potent inhibitor of the GPIb-vWF interaction and a potential novel antithrombotic agent with lower bleeding risk than GPIIb/IIIa antagonists.

Animals↗
PubMed1993

Improvement of left ventricular function after renal transplantation in a patient with uremic cardiomyopathy: report of a case.

The improvement of heart function in a patient on hemodialysis with dilated cardiomyopathy by renal transplantation is herein reported. The patient was a 35-year-old woman. Hemodialysis had been initiated 3 months before, but she experienced difficulty with hemodialysis maintenance and exhibited congestive heart failure. The ejection fraction (EF) was decreased to 36.6% in the echocardiogram, and an intracardiac biopsy of the right ventricle showed myofiber degeneration and interstitial edema upon examination by light microscopy. She then underwent renal transplantation, and the postoperative recovery was almost uneventful. The cardiothoracic ratio decreased rapidly to around 40% after 1 month, although her body weight increased. The ejection fraction increased to 50% in the echocardiogram. An intracardiac biopsy of the right ventricle revealed disoriented myofibers, but myofiber degeneration improved, and no interstitial edema was present upon examination by light microscope. The electron microscopy showed that the intracellular edema had disappeared and other degenerative changes had also improved. The patient was discharged on the 44th postoperative day, with a serum creatinine of 1.3 mg/dl.

Adult↗
PubMed1989

Synergistic deleterious effect of micromolar Ca ions and free radicals on respiratory function of heart mitochondria at cytochrome C and its salvage trial.

Both Ca2+ and free radicals (FR) are accumulated in temporarily ischemic myocardium and might cause reperfusion injury. Respiratory function measured by polarography of isolated heart mitochondria before or after the in vitro treatment with Ca2+ (1.2 microM) and/or FR showed that Ca2+ or FR per se showed no or weak effect on state 3, but cotreatment of Ca2+ and FR prominently deteriorated state 3, state 4 and RCI. The injury was speculated to occur at cytochrome c itself or its reductase from enzyme assay in the respiratory chain. Furthermore, contrary to the published data, the synergistic action was not mitigated by phospholipase A2 inhibitors (dibucaine, mepacrine), membrane stabilizers (lidocaine, coenzyme Q10), Ca entry blocker (verapamil) or superoxide dismutase, suggesting refractory to therapy.

Animals↗
PubMed1988

Protein kinase C activation aggravates hypoxic myocardial injury by stimulating Na+/H+ exchange.

The physiological and pathophysiological roles of protein kinase C activation were investigated in cultured mouse myocardial cells. First, effects of 12-O-tetra-decanoyl-phorbol-13-acetate (TPA), a potent activator of protein kinase C, on the intracellular pH (pHi) and cytosolic free Ca2+ level [( Ca2+]i) were studied, using 2',7'-bis(carboxyethyl)-5,6-carboxyfluorescein (BCECF) and quin-2, respectively. In the presence of the Ca ionophore A23187, TPA induced a rise in pHi by activating amiloride-sensitive Na+/H+ exchange and also produced a rise in [Ca2+]i above that seen with A23187 alone. These effects were totally inhibited by amiloride. Second, the effect of TPA on hypoxia-induced myocardial cell injury was evaluated. The addition of TPA to the culture medium enhanced creatine kinase release from hypoxic myocardial cells (95% N2 + 5% CO2). This effect was markedly suppressed by the addition of amiloride. These data suggests that protein kinase C activation aggravates hypoxic myocardial injury, presumably by inducing Ca2+ overload. This event is secondary to activation of Na+/Ca2+ exchange through accelerated influx of Na+ into the cells as a result of Na+/H+ exchange stimulation by protein kinase C.

Animals↗
PubMed1988

Ouabain inhibits intracellular pH recovery from acidosis in cultured mouse heart cells.

Myocardial ischaemia induces cytosolic acidification, which promotes cardiac damage, dysfunction or arrhythmia. In this study, we investigated the effect of ouabain on the intracellular pH (pHi) in cultured mouse ventricular cells, using 2',7'-bis(carboxyethyl)-5,6-carboxyfluorescein (BCECF). The average resting pHi in myocytes was 7.19. After myocytes were acid-loaded with NH4Cl, the pHi recovered from acidosis to the resting level within a few minutes via amiloride-sensitive Na+/H+ exchange. Ouabain inhibited this pHi recovery dose-dependently with half-maximal inhibition at 3 X 10(-5) M, but did not suppress the ionophore monensin-induced pHi elevation. The inhibition of the pHi recovery from acidosis by ouabain is possibly caused by an inhibition of amiloride-sensitive Na+/H+ exchange, which is secondary to a suppression of Na+ efflux through (Na+, K+) pump. Above results demonstrate the possibility that digitalis promotes intracellular acidosis or inhibits the pHi recovery from acidosis in ischaemic myocardium.

Acidosis↗
PubMed1987

Stimulated synthesis of prostaglandin E2 or leukotrien C4 from myocardial cells is not a cause but a result of their injury under hypoxia.

Cardiac muscle cell injury may be related to metabolic changes associated with a rise in intracellular calcium. The mechanisms by which an elevated Ca2+ can cause injury are uncertain, but injury could occur by activation of any one or several calcium-dependent processes. To examine whether the process is mediated by prostaglandins (PG) or leukotriens (LT), we measured the successive release of creatine kinase (CK), PGE2 and LTC4 that have been reported to induce the cell injury via the arachidonic acid cascade, to the culture medium from myocardial cells under hypoxic or aerobic conditions. CK release, a biochemical marker of muscle cell necrosis, was first detected in the medium of hypoxic cultures at 9 h. Both PGE2 and LTC4 production and release were delayed, being first detected at 12 h after initiating hypoxia treatment. Addition of exogenous PGE2 or LTC4 to the culture medium (1.0 or 10 ng/ml) did not cause any effect on the CK release under aerobic condition. Cyclooxygenase inhibitor, indomethacin (1 X 10(-5) M) or lipoxygenase inhibitor, AA861 (1 X 10(-5) M), reduced the synthesis of PGE2 by 80% or LTC4 by 68% under hypoxia, respectively, but caused no beneficial effect on the CK release. These findings suggest that cardiac muscle cells themselves produce PGE2 and LTC4 after hypoxia and that the production of these compounds merely occurs as a result, but not as a cause of cell injury.

Calcium↗