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Biomedical subjects

H Toshima

Publications and source records attributed to H Toshima.

At least 55 records · Page 3Linked to original sources
PubMed1994

Neutrophil activation after percutaneous transluminal coronary angioplasty.

We investigated whether percutaneous transluminal coronary angioplasty (PTCA) would induce neutrophil activation in patients with coronary artery disease. Blood samples were taken from the coronary sinus in 14 patients who underwent PTCA and in 9 control subjects who underwent coronary arteriography (CAG). Flow cytometry was used to measure membrane surface expression of beta 2 integrin (CD11b) and the generation of hydrogen peroxide in neutrophils after ex vivo phorbol myristate acetate stimulation by 2,'7'-dichlorofluorescein. Neutrophil elastase was measured by an immunoenzymatic method. Surface expression of CD11b increased significantly, approximately twofold, after PTCA but not after CAG. Mean fluorescence intensity of 2',7'-dichlorofluorescein in stimulated neutrophils decreased significantly after PTCA, suggesting a previous in vivo activation, but not after CAG. Neutrophil elastase increased significantly after PTCA but not after CAG. These data indicate that PTCA induces neutrophil activation and suggest that neutrophils may contribute to the ischemic injury.

Adult↗
PubMed1994

Free oxygen radicals contribute to platelet aggregation and cyclic flow variations in stenosed and endothelium-injured canine coronary arteries.

OBJECTIVES: The purpose of this study was to test the hypothesis that free oxygen radicals contribute to platelet aggregation and cyclic flow variations in stenosed and endothelium-injured coronary arteries. BACKGROUND: Although free oxygen radicals, such as superoxide anion and hydrogen peroxide, have been shown to alter platelet function in vitro, the potential role of free oxygen radicals has not been fully described in an in vivo model of coronary artery thrombosis. METHODS: Cyclic flow variations were produced in dogs by an external constrictor placed at the site of the left anterior descending coronary artery with injured endothelium. Blood flow in this artery was monitored by a pulsed Doppler flow probe. If cyclic flow variations were observed during postoperative days, dogs intravenously received superoxide dismutase plus catalase. In anesthetized dogs that did not develop an episode of cyclic flow variations, the effect of intracoronary infusion of xanthine plus xanthine oxidase or hydrogen peroxide on arterial blood flow velocity was studied. In platelet studies, the effect of free oxygen radicals and radical scavengers on platelet aggregation was examined. RESULTS: In conscious dogs with cyclic flow variations, superoxide dismutase plus catalase significantly reduced cyclic flow variations (n = 7), whereas saline infusion had no effect (n = 7). The infusion of xanthine plus xanthine oxidase or hydrogen peroxide significantly induced cyclic flow variations in four of six dogs or in five of seven dogs, respectively. In vitro platelet studies showed that xanthine plus xanthine oxidase or hydrogen peroxide significantly enhanced platelet aggregation, and superoxide dismutase or catalase significantly inhibited such aggregation. CONCLUSIONS: Reduction of free radical formation decreases platelet aggregation and may eliminate cyclic flow variations, whereas promotion of free radical generation enhances platelet aggregation and may induce cyclic flow variations. Thus, free oxygen radicals are an important mediator in this model.

Animals↗
PubMed1994

Hypertension induced by nitric oxide synthesis inhibition is renal nerve dependent.

Recent studies have indicated that chronic administration of N omega-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide (NO) synthesis, produces marked hypertension. Although the mechanism of this form of hypertension is not well understood, several studies have demonstrated that sympathetic nerve activity is at least acutely elevated after L-NAME administration. To evaluate the potential role of the renal sympathetic nerves in L-NAME-induced hypertension, we compared the blood pressure response to L-NAME in four groups of Sprague-Dawley rats (n = 8 each): (1) sham-operated vehicle-treated, (2) sham-operated L-NAME-treated, (3) denervated vehicle-treated, and (4) denervated L-NAME-treated. After renal denervation or sham surgery, L-NAME was added to the drinking water (70 mg/100 mL) for 4 weeks, and arterial pressure was measured weekly by the tail-cuff method. L-NAME treatment caused a progressive increase in arterial pressure in sham-operated rats, rising to 154 +/- 6 mm Hg by week 4 of treatment compared with 115 +/- 2 mm Hg in the vehicle-treated sham-operated group (P < .005). In contrast, the development of hypertension was significantly delayed and attenuated in renal-denervated rats treated with L-NAME. The results of our study suggest that L-NAME-induced hypertension may be partly mediated by or is at least dependent on the integrity of the renal nerves.

Animals↗
PubMed1994

Coronary artery disease trends in Japan.

Japan has experienced great socioeconomic development together with industrialization, urbanization and motorization since 1945. This has resulted in dramatic changes in both the frequency of disease and the spectrum of diseases, as well as in a rapid increase in the elderly population. Changes in eating patterns during the past 40 to 50 years seem to be a major factor in this evolution. Departure from the traditional Japanese diet, which was very high in salt and low in fat and protein (currently the diet is 25% calories from fat, 60% from carbohydrate and 15% from protein and 12 gm salt/day), has been associated with a reduced incidence of stroke, but not with an increase in coronary heart disease mortality. Therefore, the current Japanese diet may be an optimal eating pattern for maintaining health. However, since the exposure to increased fat calories is recent, future trends must be carefully monitored.

Adult↗
PubMed1994

A protease inhibitor, NCO-700, improves the contractile function in stunned canine myocardium.

To explore the role of calcium-dependent protease in the stunned myocardium, open-chest dogs underwent 15 min of left anterior descending coronary artery occlusion followed by 2 h of reperfusion. Dogs received a single bolus intravenous injection of either the protease inhibitor NCO-700 (n = 6) or saline (n = 6) 1 min before reperfusion followed by a 30-min infusion at the same dose. Regional myocardial function was assessed in terms of systolic wall thickening with an epicardial Doppler probe. The two groups exhibited comparable systolic thickening under baseline conditions and similar degrees of dyskinesis during occlusion. After reperfusion, recovery of contractile function, expressed as a percentage of the baseline value, was significantly greater in NCO-700-treated dogs as than in control dogs: -14.3 +/- 10.6 vs -48.9 +/- 7.2 (p < 0.05) at 15 min, 10.8 +/- 10.3 vs -31.1 +/- 9.0 (p < 0.05) at 30 min, 42.5 +/- 10.1 vs -16.4 +/- 9.1 (p < 0.005) at 1 h, and 47.5 +/- 8.3 vs -14.9 +/- 9.4 (p < 0.001) at 2 h. The data suggest that the protease inhibitor markedly improved contractile function in stunned myocardium by inhibiting intracellular protease activity.

Animals↗
PubMed1994

Soluble form of P-selectin in patients with acute myocardial infarction.

BACKGROUND: P-selectin, an integral membrane glycoprotein of platelets and endothelial cells, is rapidly redistributed to the cell surface after cellular activation. The soluble form of P-selectin has been shown to be present in people with normal circulation. The purpose of the present study was therefore to examine the soluble form of P-selectin in patients with acute myocardial infarction (AMI). METHODS: Whole blood was obtained from nine patients with AMI and from 10 volunteers who made up the control group. Plasma concentrations of the soluble form of P-selectin were examined with a monoclonal antibody-based enzyme immunoassay. RESULTS: Plasma P-selectin levels in control volunteers were 178 +/- 44 ng/ml. In patients with AMI, plasma P-selectin levels on days 1, 2 and 3 were 743 +/- 374, 627 +/- 267, and 588 +/- 223 ng/ml, respectively (P < 0.001)--significantly higher than the levels in the control volunteers. CONCLUSION: Plasma concentrations of the soluble form of P-selectin were markedly higher in patients with AMI, suggesting the activation of platelets, or endothelial cells, or both. Thus, quantitative measurements of plasma P-selectin concentrations may help to assess the pathophysiology of inflammatory reactions in patients with AMI.

Adult↗
PubMed1994

[Detection and localization of multiple metastases from differentiated thyroid carcinoma with 99mTc-MIBI whole body scintigraphy: a case report].

A 79-year-old male with a history of total thyroidectomy due to follicular thyroid carcinoma developed multiple metastases in the lung, bone, and lymph nodes. In order to detect and localize every metastases, 99mTc-MIBI whole body scintigraphy was performed, and clearly depicted all metastatic lesions except tiny pulmonary nodules. 99mTc-MIBI whole body scintigraphy may be useful in detecting metastases from differentiated thyroid carcinoma, because of a good quality of scintigram and no need of patient preparation. This article is the first report on 99mTc-MIBI localization in multiple metastases from differentiated thyroid carcinoma.

Adenocarcinoma, Follicular↗
PubMed1993

A deletion of mitochondrial DNA in murine doxorubicin-induced cardiotoxicity.

A deletion of about 4 kb has been determined in the mutated mitochondrial DNA (mtDNA) in cardiomyocytes with chronic doxorubicin (DOX)-induced cardiotoxicity in mouse. The incidence of the mtDNA deletion increased with the dosage and with the duration of the DOX administration. Coenzyme Q10 administration prevented the mtDNA deletion and decreased the thiobarbituric acid reactive substance content in the heart mitochondria, suggesting some free radical involvement in this mtDNA deletion. This mtDNA deletion may be involved in cardiomyopathy, which is known to be dosage-dependently induced by DOX administration.

Animals↗
PubMed1993

A missense mutation of cardiac beta-myosin heavy chain gene linked to familial hypertrophic cardiomyopathy in affected Japanese families.

A novel missense mutation of the cardiac beta-myosin heavy chain gene was detected in five unrelated Japanese patients and their affected family members with hypertrophic cardiomyopathy (HCM) by using the polymerase chain reaction (PCR)-DNA conformation polymorphism (DCP) analysis. Sequencing analysis revealed an A to G transition at codon 778 leading to replacement of the Asp residue, which is adjacent to the interaction sites of myosin heavy chain (MHC) with actin and is a conserved amino acid residue in various MHC across species, to the Gly residue. Linkage study of the mutation and two dinucleotides repeat markers of the cardiac beta-MHC gene in three affected families showed that the mutation was on the same haplotype of the cardiac beta-MHC gene and linked to HCM. These observations strongly suggest that the 778Asp to Gly mutation is the cause of HCM in these affected individuals.

Actins↗
PubMed1993

Cyclic flow variations in a conscious dog model of coronary artery stenosis and endothelial injury correlate with acute ischemic heart disease syndromes in humans.

OBJECTIVES: The purpose of this study was to test the hypothesis that episodes of cyclic flow variations (CFVs) in conscious dogs with coronary stenoses and endothelial injury correlate with acute ischemic heart disease syndromes in humans. BACKGROUND: Although the canine model with CFVs has proved to be a useful model of coronary thrombosis, whether CFVs progress to these syndromes has not been clearly described. METHODS: Cyclic flow variations were produced by an external constrictor placed at the site of the left anterior descending coronary artery with injured endothelium. Blood flow in this artery and 24-h Holter electrocardiogram (ECG) were recorded during the 1st 5 postoperative days. RESULTS: Of 41 dogs that underwent the initial operative procedure successfully, 29 developed an episode of CFVs. In five dogs in which CFVs persisted throughout the monitoring period, the left anterior descending coronary artery flow decreased until day 3 and thereafter increased through day 5. Transient coronary occlusion during CFVs induced ST segment changes that returned to baseline after reflow. In 12 dogs, CFVs progressed to persistent coronary occlusion, and histologic examination revealed thrombus formation at the stenotic site and evidence of myocardial infarction. Four of these 12 dogs died suddenly of ventricular arrhythmias during persistent coronary occlusion; another 5 dogs died of reperfusion arrhythmias during CFVs with no evidence of myocardial infarction. CONCLUSIONS: Conscious dogs with CFVs closely correlated with clinical acute ischemic heart disease syndromes, suggesting them to be a useful model for investigating the complex mechanisms of cellular interactions in the pathogenesis of these syndromes.

Animals↗
PubMed1993

Alterations in beta-adrenergic receptor density and cyclic-AMP level in the myocardium of rats chronically treated with alcohol.

An impaired function of the myocardial beta-adrenergic receptor system has been reported in patients with end-stage heart failure and this impairment has been postulated to be a factor in further deterioration of cardiac contractile function. As ventricular dysfunction is often associated with prolonged alcohol abuse, we investigated whether or not chronic administration of ethanol could induce alterations in the beta-adrenergic receptor adenylate-cyclase system in rats. Male Wistar rats of 8 weeks of age received 33% ethanol in drinking water for 3 months. As compared with control rats drinking water, the ethanol-treated rats showed weight loss and an increase in the heart/body weight ratio. Chronic ethanol increased myocardial contents of norepinephrine and epinephrine, possibly resulting from sympathoadrenal activation. The beta-adrenergic receptor density (Bmax) of the myocardial membrane was significantly decreased in the ethanol-treated rats (27.7 +/- 9.9 vs 39.0 +/- 6.0 fmol/mg protein, p < 0.01), while the affinity (Kd) did not differ between the two groups. The myocardial content of cyclic-AMP was also reduced in the ethanol rats (865 +/- 59 vs 1055 +/- 83 pmol/g w.w., p < 0.01). These observations indicate that chronic ethanol administration depresses the function of the beta-adrenergic receptor adenylate-cyclase system. The decreased beta-adrenergic receptor density was partly attributed to down-regulation due to increased sympathetic stimulation. This impaired function may contribute to the cardiac contractile dysfunction observed in chronic alcoholics.

Animals↗
PubMed1993

Evaluation of the intramembrane particle count in biopsied myocardium from patients with idiopathic cardiomyopathy.

To clarify the abnormalities of myocardial membrane structure in cardiomyopathy, the density of intramembranous particles (IMP) of mitochondria, sarcoplasmic reticulum and sarcolemma, and the number of caveolar necks was evaluated by freeze-fracture morphology. The subjects consisted of 17 patients with hypertrophic cardiomyopathy (HCM), 6 patients with dilated cardiomyopathy (DCM), and 7 patients as controls. The results showed that the numbers of IMPs on the membrane faces of mitochondria, sarcoplasmic reticulum and sarcolemma were significantly decreased in HCM and DCM, and that they were decreased more markedly in DCM than in HCM. The number of caveolar necks was significantly decreased in DCM. Thus, the decreased numbers of IMPs on myocardial membranes and the decrease in caveolar necks may be important characteristics resulting from abnormal myocardial membrane metabolism in cardiomyopathies, HCM and DCM.

Adult↗
PubMed1993

Prognostic significance of electrocardiographic findings in patients with dilated cardiomyopathy.

The prognostic significance of electrocardiographic variables was retrospectively investigated in 88 patients with dilated cardiomyopathy and with normal coronary arteriograms. During an average follow-up of 3.7 +/- 2.9 years, 43 patients died, 26 of progressive heart failure, 15 patients with sudden death, and one due to cerebral embolism. Excluding one patient, who died of esophageal cancer, the cumulative survival rate was 73% at 2 years and 60% at 5 years. By univariate life table analysis, abnormal Q-waves, a QRS duration > or = 0.12s, a cardiothoracic ratio > or = 60%, systolic blood pressure < 110mmHg, and left ventricular end-diastolic pressure > or = 15mmHg were significantly associated with increased mortality within 5 years. Multivariate analysis using Cox's proportional hazards model determined the major independent risk factors in the following order: (1) for all patients; the presence of abnormal Q-waves, left bundle branch block or intraventricular conduction disturbances, left ventricular end-diastolic pressure, systolic blood pressure and the cardiothoracic ratio; (2) for patients without left bundle branch block or intraventricular conduction disturbances; abnormal Q-waves, left ventricular end-diastolic pressure and systolic blood pressure. The present study thus demonstrated that the electrocardiogram could provide independent prognostic predictors in patients with dilated cardiomyopathy, possibly reflecting the severity of myocardial damage.

Cardiomyopathy, Dilated↗
PubMed1993

[A study of myocardial disorders in an autopsy case of mitochondrial encephalomyopathy].

We report an autopsy case of a 19 year-old man with MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes) a subgroup of mitochondrial encephalomyopathy presenting cardiomyopathy. He had repeatedly suffered from transient unconsciousness, hemiplegia, hemianopsia and convulsion attacks since the age of 9, and he died of severe congestive heart failure. In laboratory findings, blood lactate and pyruvate were markedly increased. Skeletal muscle biopsy demonstrated numerously scattered ragged-red fibers with modified Gomori's trichrome staining. Enzymatic activities of the mitochondrial respiratory chain showed a marked decrease of NADH cytochrome c reductase (complex I). In postmortem examination, the heart was 310g in weight and had right ventricular dilatation. Microscopically, degenerated and scattered myocardial cells (ragged-red fibers), interstitial edema and microvascular hyperplasia were demonstrated in the myocardium. Under the electron microscope, abnormal mitochondria proliferated and myofibrils were unusually sparse. Immunohistochemical studies with specific antibodies against the mitochondrial electron transfer enzyme subunits revealed a reduction of immunoreactive materials for complex I in the myocardium. These results suggested the relationship of myocardial disorders and decreased activity of complex I in electron transfer enzymes in this patient.

Adult↗
PubMed1992

Adult coronary artery disease probably due to childhood Kawasaki disease.

We have surveyed adult survivors of childhood Kawasaki disease (KD) who had coronary artery disease that could be ascribed to KD. In response to questionnaires sent to cardiologists throughout Japan, 21 patients (17 men, 4 women, aged 20-63 years) with coronary lesions and a definite (2) or suspected (19) history of KD were reported. 5 patients had presented with acute myocardial infarction, 6 previous myocardial infarction, 9 angina pectoris, and 1 dilated cardiomyopathy. 16 patients had obstructions in two or more coronary arteries. 3 had died and 18 were alive with serious sequelae (mitral regurgitation, arrhythmias, congestive heart failure). Childhood KD should be included in the differential diagnosis of coronary artery disease in young adults.

Adult↗