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T Hano

Publications and source records attributed to T Hano.

At least 19 recordsLinked to original sources
PubMed2001

Method for measuring mutagen formation potential (MFP) on chlorination as a new water quality index.

A novel water quality index, the mutagen formation potential (MFP) is proposed for use in evaluation of the quality of drinking water which may contain pollutants capable of forming mutagens when chlorinated under the conditions used in water purification processes. A method for measuring MFP was established as follows. The water sample to be tested is diluted until the TOC reaches 3-4 mg l-1, the pH is adjusted to 7.0 +/- 0.2, sodium hypochlorite is added to obtain conditions where Cl/TOC = 3-4 mg Cl (mg C)-1, and the water sample is left standing for 24 +/- 2 h at room temperature. Thereafter, 21 of the chlorinated water sample at pH 2.0 +/- 0.1 is passed through a Sep-Pak Plus CSP-800 cartridge to adsorb any mutagens formed, and DMSO is applied to the cartridge to desorb the mutagens. Then, a 2 ml sample of the eluate is collected after the DMSO had begun to flow out of the cartridge and evaluated by the Ames Salmonella mutagenicity assay (preincubation method).

Chlorine Compounds↗
PubMed2001

Usefulness of saturation pulses in magnetic resonance imaging of partial anomalous pulmonary venous return.

The authors evaluated partial anomalous pulmonary venous return by magnetic resonance (MR) images. Seven patients with this congenital anomaly underwent MR imaging examination. Conventional spin-echo and gradient-echo imaging were performed. In addition, during acquisition of gradient-echo images, saturation pulses were imposed on the affected lung. Spin-echo images showed the anatomical situation of the anomalous veins, and gradient-echo images revealed the blood flow in the veins. With saturation technique, the direction and drainage of blood flow in the anomalous veins were well defined. The study suggests that MR imaging with spin-echo method and gradient-echo method with or without saturation pulses is a useful and noninvasive method of diagnosing partial anomalous pulmonary venous return. MR images with spin- and gradient-echo methods were useful in defining the anatomical situation and blood flow in the anomalous veins. By imposing saturation pulses on the affected lung field, the direction and drainage of blood flow in the anomalous veins were clearly demonstrated.

Adolescent↗
PubMed2001

Apoptosis of vascular smooth muscle cells is induced by Fas ligand derived from endothelial cells.

Although Fas-mediated cell death may play a role in atherogenesis, causal data in support of this hypothesis are lacking. The present study investigated the possibility that endothelial cells are involved in vascular smooth muscle cell (VSMC) apoptosis via the Fas-FasL pathway, and hence in atherogenesis. FACS analysis detected FasL on the surface of human umbilical vein endothelial cells (HUVECs) and immunofluorescence staining of the HUVECs demonstrated high levels of FasL in the intracellular compartment. FasL was down-regulated 4 h after tumor necrosis factor (TNFalpha) treatment, coinciding with maximal surface expression of the adhesion molecules vascular cell adhesion molecule-1 and E-selectin. However, the down-regulation of FasL expression was transient, as surface expression returned within 24 h of TNFalpha treatment. When cocultured with VSMCs, the FasL-expressing EC could kill the VSMCs in a manner that could be blocked by recombinant Fas-Fc, deployed as a soluble receptor for Fas. Moreover, when human coronary arteries were studied with immunohistochemistry using G247-4 monoclonal antibody for the detection of FasL, few FasL positive EC were observed in diffuse intimal thickening. In contrast, endothelium overlying the plaque showed prominent and uniform expression of FasL. These findings suggest that the Fas/FasL pathway can be used by EC to induce VSMC apoptosis in the atherosclerotic lesion.

Adult↗
PubMed2001

[Treatment of hypertension in the patients with obesity].

Obesity is often accompanied with hypertension and increases cardiovascular events. Japanese new guideline on identification of obesity includes a modified BMI categories and a method of detection of visceral fat obesity in Japanese. Hyper-insulinemia and leptin released from adipose tissue play an important role in the development of hypertension in obese patients. Insulin and leptin increase sympathetic tone which results in sodium retention and hyper-responsiveness of blood vessels. As leptin has also a direct vasodilative and diuretic action, its effect on blood pressure is bidirectional. Life style modification, especially diet and physical exercise are important to obtain the body weight loss and the improvement of insulin resistance. Dynamic exercise at the level of fifty percent of max VO2 for 30 to 60 minutes over three times a week should be recommended for hypertensive patients with obesity. ACE inhibitors improve the hypersympathetic tone and impaired insulin sensitivity in obese patients. Calcium antagonist is also useful for these patients.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2000

Involvement of nitric oxide in endothelium-dependent arterial relaxation by leptin.

Leptin is a polypeptide, mainly produced in white adipose tissue, and increases sympathetic nerve activity. A few studies investigated leptin's effect on peripheral vessels. We examined the vasorelaxant effects of human leptin on rat arteries. Arterial rings were precontracted with 1 x 10(-6) mol/l of phenylephrine, and leptin was superfused. Leptin relaxed phenylephrine-precontracted arterial rings in a dose-dependent manner. ED50 was calculated to 8.4 microg/ml. Removal of endothelium abolished the effects of leptin. Indomethacin (1 x 10(-5) mol/l) did not affect the vasorelaxation by leptin, whereas 1 x 10(-4) mol/l of N(omega)-nitro-L-arginine methyl ester (L-NAME) completely suppressed it. The inhibition was antagonized by 1 x 10(-4) mol/l of L-arginine. Leptin normally relaxed arterial rings during superfusion of K channel blockers, including 3 x 10(-5) mol/l of glibenclamide, 1 x 10(-6) of mol/l apamin, and 5 x 10(-7) mol/l of charybdotoxin. Low Cl(-) solution (8. 3 mmol/l) inhibited leptin-induced relaxation, but endothelium-independent vasodilatation by nitroprusside was not impaired at low Cl(-) solution. These results suggest that arterial relaxation by leptin is mediated by nitric oxide released from endothelium, and Cl(-) plays an important role in leptin-induced nitric oxide release.

Acetylcholine↗
PubMed2000

Cellular FLIP is expressed in cardiomyocytes and down-regulated in TUNEL-positive grafted cardiac tissues.

OBJECTIVE: c-FLIP is a natural homologue of caspase 8, and may antagonize activation of death pathways mediated by FADD. c-FLIP is highly expressed in the heart, and a recent report suggests that c-FLIP may protect against certain types of myocyte death. The present study was designed to define the expression patterns of c-FLIP in the heart. METHODS: The expression pattern of c-FLIP in end-stage human hearts, and rat cardiomyocyte grafting models was analyzed by in situ hybridization, immunohistochemistry and TUNEL assay. In addition, to determine whether Fas-dependent pathway is active in cardiomyocytes in vitro, we examined whether activated monocytes can kill neonatal cardiomyocytes in a co-culture system. RESULTS: c-FLIP mRNA and protein were abundantly expressed in normal cardiomyocytes from failing human heart. In animal models, c-FLIP protein was absent in TUNEL-positive grafted cardiomyocytes. Double staining demonstrated that c-FLIP-positive cells rarely had fragmented DNA, while TUNEL-positive cells rarely contained c-FLIP. Finally, activated monocytes induced death of neonatal rat cardiomyocytes via the Fas/FasL system. CONCLUSIONS: Loss of c-FLIP expression correlates with cardiomyocyte cell death. We hypothesize that diminished c-FLIP expression may predispose cardiomyocytes to apoptotic death.

Adult↗
PubMed2000

Conserved smooth muscle contractility and blood pressure increase in response to high-salt diet in mice lacking the beta3 subunit of the voltage-dependent calcium channel.

Voltage-dependent calcium channels are crucially important for calcium influx and the following smooth muscle contraction. Beta subunits of these channels are known to modify calcium currents through pore-forming alpha subunits. Among the four reported independent beta subunits, the beta3 subunit is expressed in smooth muscle cells and thought to compose L-type calcium channels in the tissue. To determine the role of the beta3 subunit in the cardiovascular system, we have analyzed beta3-null mice. Electrophysiological examinations proved the existence of dihydropyridine (DHP)-sensitive. L-type calcium channels in the smooth muscle cells. Beta3-null mice show no apparent changes in smooth muscle contraction and sensitivity to DHP, and normal blood pressure when they are raised on a normal diet, but the 13 subunit deficient mice show elevated blood pressure in response to a high-salt diet, with significant reductions in plasma catecholamine concentrations. Our finding strongly suggests a close relationship between voltage-dependent channels and high blood pressure.

Animals↗
PubMed2000

Diabetic ketoacidosis associated with Guillain-Barré syndrome with autonomic dysfunction.

A 37-year-old woman was admitted in a comatose state, after exhibiting fever and diarrhea. Diabetic ketoacidosis was diagnosed due to an increased blood glucose level (672 mg/dl), metabolic acidosis, and positive urinary ketone bodies. On the fifth hospital day, despite recovery from the critical state of ketoacidosis, the patient suffered from dysphagia, hypesthesia and motor weakness, followed by respiratory failure. Cerebrospinal fluid analysis was suggestive of Guillain-Barre syndrome (GBS). Autonomic dysfunction was manifested as tachycardia and mild hypertension in the acute stage. Marked orthostatic hypotension persisted long after paresis was improved, indicating an atypical clinical course of GBS.

Adult↗
PubMed2000

[Catecholamine].

Explore the source record for details and available documents.

Catecholamines↗
PubMed1999

Dynamic outflow obstruction due to the transient extensive left ventricular wall motion abnormalities caused by acute myocarditis in a patient with hypertrophic cardiomyopathy: reduction in ventricular afterload by disopyramide.

A 65-year-old woman was admitted to the coronary care unit because of acute pulmonary edema. Immediate 2-dimensional and Doppler echocardiograms revealed extensive left ventricular wall motion abnormalities and left ventricular hypertrophy with extreme outflow obstruction. Although an ECG showed ST-segment elevation in the anterolateral leads, a coronary arteriogram revealed normal epicardial arteries. Heart failure was relieved after diminishing the dynamic outflow obstruction with disopyramide administration. An endomyocardial biopsy from the right ventricle on the 8th hospital day showed borderline myocarditis. Wall motion abnormalities gradually normalized within 2 weeks. It is speculated that her pulmonary edema would not have been relieved so readily without the immediate reduction in ventricular afterload by disopyramide. These clinical changes over time were observed with serial echo-Doppler examinations.

Acute Disease↗
PubMed1999

Arterial relaxation mediated by endothelium-derived hyperpolarizing factor in hypertension induced by chronic inhibition of nitric oxide synthesis.

The aim of this study was to evaluate arterial relaxation mediated by endothelium-derived hyperpolarizing factor (EDHF) during chronic inhibition of nitric oxide (NO) synthase. We measured the isometric tension of isolated mesenteric arteries of Wistar rats administered Nomega-nitro-L-arginine methyl ester (L-NAME, 100 mg/Kg/day) for 3 weeks. Relaxation to acetylcholine (ACh) was reduced in L-NAME treated rats (maximum relaxation, 52% versus 79% ). After acute superfusion of 1x10(-4) M L-NAME, half the relaxation was inhibited in controls, while the relaxation was not changed in L-NAME treated rats. In contrast, relaxation to nitroprusside was normal in L-NAME treated rats. Superfusion of 1x10(-6) M apamin, which inhibits the effects of EDHF, reduced the relaxation. The relaxation inhibited by apamin was not significantly different between the two groups. These findings suggested that in endothelial cells, the synthesis of EDHF is unchanged during a chronic deficiency of relaxation influence of NO.

Acetylcholine↗
PubMed1998

Enhanced efficacy of nilvadipine in hypertensives whose raised ambulatory blood pressure is sustained during sleep.

This study was designed to clarify the relationship between the antihypertensive effects of the calcium antagonist nilvadipine, and circadian changes in blood pressure. Based on measurements using an ambulatory blood pressure monitoring system (ABPM), 17 outpatients with untreated essential hypertension were divided into two groups: a sustained hypertensive group (with a fall in blood pressure during sleep < 10%, n = 7) and a waking time hypertensive group (with a fall in blood pressure during sleep > or = 10%, n = 10). During treatment with nilvadipine (8 mg/day, > or = 2 weeks), patients were reexamined by ABPM. The antihypertensive effect of nilvadipine was significantly and negatively correlated with the night time fall in blood pressure: this effect was significantly greater in the sustained hypertensive group than in the waking time hypertensive group. These data suggest that the long acting calcium antagonist nilvadipine has more potent antihypertensive effects in patients with sustained hypertension ("nondippers") than in those whose hypertension lessens during sleep ("dippers").

Aged↗
PubMed1998

A premenopausal woman presenting with acute myocardial infarction of three different coronary vessels within 1 year: role of lipoprotein(a).

A premenopausal female patient presented with acute myocardial infarction of 3 different coronary vessels at different times within 1 year. These events were caused not by restenotic lesions after balloon angioplasty but by new lesions, which were successfully treated by primary angioplasty. Although she had a history of hypertension, type IIB hyperlipidemia, and diabetes, they had been well-controlled on medication. An elevated serum lipoprotein(a) level may have played a role in this rapid angiographic progression.

Angioplasty, Balloon↗
PubMed1998

Pulmonary capillary hemangiomatosis: a unique feature of congestive vasculopathy associated with hypertrophic cardiomyopathy.

A 34-year-old man with an 18-year history of hypertrophic cardiomyopathy died of worsening right-sided heart failure. Central venous pressure was greatly increased to 25 cm H2O before death. Postmortem examination revealed features of severe congestive vasculopathy, including those of pulmonary capillary hemangiomatosis in the lungs. Marked proliferation of capillaries was seen chiefly in alveolar septa and extending into pulmonary veins and arteries, causing severe luminal occlusion with recanalization. Diffusely distributed intra-alveolar edema and hemorrhage with collections of hemosiderin-laden macrophages were also seen, which suggested that the pulmonary capillary hemangiomatosis was associated with longstanding chronic passive congestion of the lung. It is possible that severe pulmonary passive congestion may be one of the causes of development of idiopathic pulmonary capillary hemangiomatosis.

Adult↗
PubMed1997

Increased Ca2+ sensitivity of contractile elements via protein kinase C in alpha-toxin permeabilized SMA from young spontaneously hypertensive rats.

OBJECTIVE: The purpose of the present investigation was to examine the Ca2+ sensitivity of the contractile elements via protein kinase C (PKC) in superior mesenteric artery (SMA) from young (5-6 weeks old) spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). METHODS: Staphylococcal aureus alpha-toxin, which produces pores in the plasma membrane too small to allow passage of proteins such as PKC, was used to investigate the signal transduction system in vascular smooth muscle cells. We investigated the Ca2+ sensitivity of the contractile apparatus via PKC in intact and alpha-toxin skinned SMA from young SHR and WKY. RESULTS: In intact SMA, high K+ responses were not different between SHR and WKY. However, phorbol 12,13-dibutyrate (PDBu, a PKC activator) augmented high K(+)-evoked contractions and PKC inhibitors, such as 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7) and calphostin C, suppressed them more in SHR as compared with WKY. In alpha-toxin skinned SMA, the [Ca2+]i-force relationship curve was not significantly different between SHR and WKY. However, PDBu augmented [Ca2+]i-evoked contractions and PKC inhibitors suppressed them more in SHR than in WKY. CONCLUSION: These results suggest that the Ca2+ sensitivity of the contractile elements via PKC is significantly greater in prehypertensive SHR than in age-matched WKY. This abnormality in small muscular arteries may be involved in the pathogenesis of hypertension in SHR.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1997

Effects of locally administered argatroban on restenosis after balloon angioplasty: experimental and clinical study.

1. This study was undertaken to evaluate the preventive effects of locally administered argatroban, a competitive inhibitor of thrombin-induced platelet activation, on restenosis after balloon angioplasty. 2. A hydrogel-coated balloon catheter was immersed three times in argatroban/saline solution (1 mg/mL) for 60 s, inflated to a pressure of 606 kPa and left in the rabbit common carotid artery for 1 min. The same procedure was performed, without drug, as a control. The pharmacokinetics of delivered argatroban in the arterial wall were assessed using [14C]-argatroban. Platelet deposition 2 h after balloon injury was quantified by fluorescence studies using antiplatelet antibody. Vascular smooth muscle cell (VSMC) proliferation 3 days after balloon injury was assessed by immunohistochemical staining for proliferative cell nuclear antigen (PCNA). In a clinical study, we divided 50 elective patients into two groups: argatroban and control. 3. In the experimental study, the mean quantities of argatroban at 0, 2 and 6 h after deflation were 24.63, 0.49 and 0.11 nmol/g wet weight of artery, respectively. Argatroban was undetected 24 h after deflation. Two hours after deflation, argatroban-treated arteries showed less platelet adhesion than saline-treated controls. The mean number of PCNA-positive cells was 16.9 and 43.8% in the argatroban and control groups, respectively (P < 0.01). In the clinical study, the mean late gain loss was 8.2 and 27.3% in the argatroban and control groups, respectively (P < 0.05). The mean late restenosis rate was 11.1 and 41.4% in the argatroban and control groups, respectively (P < 0.05). 4. These data suggest that blood coagulation plays a significant role in VSMC proliferation after balloon injury and that locally administered argatroban using hydrogel-coated balloon catheter may prevent post-percutaneous transluminal coronary angioplasty restenosis.

Angioplasty, Balloon↗
PubMed1997

Effects of locally administration of argatroban using a hydrogel-coated balloon catheter on intimal thickening induced by balloon injury.

The purpose of this study was to evaluate the inhibitory effects of locally delivered argatroban, a competitive inhibitor of thrombin-induced platelet activation, on intimal proliferation after balloon injury. A hydrogel-coated balloon catheter was immersed 3 times in an argatroban/saline solution (1, 0.1, or 0.01 mg/ml) for 60 s and inflated at 6 atm pressure for 1 min in the rabbit common carotid artery. Immersion in a saline solution without drug followed by the same procedure served as a control. Accumulation of argatroban in the vascular wall was confirmed by chemical determination using high-performance liquid chromatography (HPLC). The concentration of argatroban in the vessel wall immediately after deflation after balloon immersion in solutions of 1 and 0.1 mg/ml was 14.8 +/- 10.9 and 5.5 +/- 4.6 nmol/g wet weight of artery, respectively. Argatroban was not detected in arteries treated with a balloon that had been immersed in the 0.01 mg/ml argatroban/saline solution. Intima-media area ratios 20 days after balloon injury in the groups treated with 1 mg/ml (n = 8) and 0.1 mg/ml (n = 6) agratoban were significantly smaller than that in the groups treated with 0.01 mg/ml (n = 7) argatroban or saline (n = 8) (0.35 +/- 0.11, 0.50 +/- 0.17, 1.24 +/- 0.39, and 1.35 +/- 0.43, respectively; p < 0.001). These data suggest that locally administered argatroban dose-dependently inhibits intimal thickening in a rabbit model of carotid artery injury.

Angioplasty, Balloon, Coronary↗