[Drugs for the heart failure].
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Adrenergic beta-Antagonists↗
Biomedical subjects
M Kohno
Publications and source records attributed to M Kohno.
[Primary biliary cirrhosis, rheumatoid arthritis and Sjögren's syndrome following implantation of ventriculoperitoneal shunt tube--an aged male case report].
A 73-year old male was received implantation of ventriculoperitoneal shunt tube (made with silicone) following subarachnoid hemorrhage in March 1991. Alkaline phosphatase was elevated gradually and he was diagnosed as having primary biliary cirrhosis by antimitochondria antibody and liver biopsy. He had been taking urso acid after that time on. He was admitted to our hospital because of stiffness and edema of both hands in November 1993. He was diagnosed as rheumatoid arthritis by morning stiffness with duration of few hours bilateral swelling of metacarpal, proxymal intrapharangeal and wrist joints and positive rheumatoid factor. In addition he felt dry mouth and laboratory data revealed that antinuclear antibody was 640x, centromere type, anti-SS-A antibody positive and elevation of circulating immune complex. A salivary gland disfunction was showed by gum test and salivary gland scintigraphy. Therefore the diagnosis of Sjögren's syndrome was made also. Connective tissue diseases have been reported to occur following cosmetic surgery with injection of the foreign substances paraffin and silicone. Now it is supposed to be the first case tcat connective tissue disease following ventriculoperitoneal shunt tube implantation.
Aged↗
Relationship between the regression of left ventricular hypertrophy and the changes in circadian blood pressure after long-term treatment with enalapril in hypertensive patients.
The ambulatory blood pressure (BP) was recorded for 24 hours in 28 untreated hypertensive patients, and mean values of systolic (SBP) and diastolic BP (DBP) were measured over 24 hours, during the day-time (6:00 to 19:30), and during the night-time (20:00 to 5:30). M-mode echocardiography was performed and several parameters of left ventricular size were calculated. In addition, 13 men of 18 patients with left ventricular hypertrophy (LVH) received long-term treatment with enalapril, and ambulatory BP monitoring and echocardiographic measurement were performed in 10 of these patients 6 months after active treatment ended. In all 28 patients, left ventricular mass index (LVMI) was significantly related to 24-hour, day-time and night-time SBP. Other parameters of hypertrophy were correlated with 24-hour and/or night-time BP, but not with day-time BP. In patients with LVH, night-time DBP was significantly higher and the night-time decline in DBP was significantly less than in those without LVH. The 6-month treatment with enalapril clearly decreased casual and ambulatory BP and reduced LVMI. The reduction of LVMI was strongly correlated with the decrease in night-time SBP and DBP compared with the decrease in day-time BP. These observations indicate that LVH is related to 24-hour BP (especially night-time BP) and that the regression of this condition may be related to a decline in night-time BP.
Adult↗
[Bronchial hypersensitivity in Sjögren's syndrome].
It has been reported that Sjögren's syndrome has various pulmonary involvement including lymphoid interstitial pneumonia, lung fibrosis and various pulmonary manifestation. And some abnormalities in respiratory function have been pointed out. Bronchial hypersensitivity has been indicated in patients with bronchial asthma. It has been revealed that it plays an important role in pathogenesis of bronchial asthma. Recently, some authors reported bronchial hypersensitivity in patients with Sjögren's syndrome. We studied bronchial responsiveness to methacholine by using astograph in patients with Sjögren's syndrome. The patients are 25 subjects with Sjögren's syndrome. Bronchial hypersensitivity was seen in 15 patients (60%). And it's pattern was more slight than it of bronchial asthma patients. Our results show bronchial hypersensitivity in Sjögren's syndrome which has been pointed out recently. It may be due to an alteration of bronchial epithelium secondary to lymphocytic inflammation and damage of bronchial glands.
Adolescent↗
Dynamic observation of Si crystal growth on a Si(111)7 x 7 surface by high-temperature scanning tunneling microscopy.
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Journal Article↗
Preliminary investigation of crystals of lipase I from Rhizopus niveus.
Lipase I from Rhizopus niveus consists of two polypeptide chains bound non-covalently. Lipase I has been crystallized in a form suitable for X-ray diffraction analysis using the hanging drop method of vapour diffusion at 20 degrees C. The crystals grew at pH 6.0 to 7.0 using 14 to 16% polyethylene glycol 8000 as the precipitant. The crystals are tetragonal with space group P4(1) (or P4(3)) and cell dimensions of a = b = 83.7 A, c = 137.9 A. There are two protein molecules in the asymmetric unit. The diffraction pattern extends to at least 2.5 A resolution.
Lipase↗
Tumor necrosis factor stimulates the synthesis and secretion of biologically active nerve growth factor in non-neuronal cells.
Tumor necrosis factor-alpha (TNF) markedly stimulates the synthesis and secretion of immunoreactive nerve growth factor (NGF) in quiescent mouse fibroblasts, which is a result of increase in the NGF mRNA level. NGF produced by TNF-treated fibroblasts has a molecular mass of 13 kDa on SDS-polyacrylamide gel electrophoresis, which is consistent in size with the subunit of mouse beta-NGF, and induces neurite outgrowth in paravertebral sympathetic neurons. Several peptide growth factors such as basic fibroblast growth factor (bFGF) and epidermal growth factor also stimulate NGF production in the cells, but not platelet-derived growth factor. The dose responses of TNF and bFGF to stimulate NGF production in the cells are, respectively, similar to those to induce cell proliferation. However, no correlation is observed between the ability of these growth factors to stimulate NGF production and that to induce cell proliferation. Thus, the stimulation of NGF production in the cells seems to be a specific activity of TNF and some other growth factors. TNF stimulates the synthesis and secretion of NGF also in other cells such as human glioblastoma cells. These findings suggest that TNF plays a role in regulating neuronal cell function through an indirect mechanism by which it stimulates NGF production in glial cells and fibroblasts.
3T3 Cells↗
Generation of hydroxyl radical from lipid hydroperoxides contained in oxidatively modified low-density lipoprotein.
When low-density lipoprotein (LDL) was oxidatively modified and incubated with an epinephrine-FeCl3 mixture, an electron spin resonance spectrum characteristic of the spin adduct of 5,5-dimethyl-1-pyrroline-N-oxide and hydroxyl radical (DMPO-OH) was obtained. The amount of DMPO-OH formed increased with an increase in the concentration of lipid hydroperoxides contained in the oxidatively modified LDL. These results indicate that oxidatively modified LDL would generate hydroxyl radicals in vivo if an appropriate iron chelate were present and that the cytotoxicity of oxidatively modified LDL is ascribable, at least in part, to its capability to generate such radicals.
Animals↗
Antagonistic action of imidazolineoxyl N-oxides against endothelium-derived relaxing factor/.NO through a radical reaction.
A labile inorganic free radical, nitric oxide (.NO), is produced by nitric oxide synthase from the substrate L-arginine in various cells and tissues. It acts as an endothelium-derived relaxing factor (EDRF) or as a neurotransmitter in vivo. We investigated the reactivity of stable radical compounds, imidazolineoxyl N-oxides such as 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl 3-oxide (PTIO), carboxy-PTIO, and carboxymethoxy-PTIO against .NO/EDRF in both chemical and biological systems. By using electron spin resonance (ESR) spectroscopy, imidazolineoxyl N-oxides were found to react with .NO in a stoichiometric manner (PTIO/.NO = 1.0) in a neutral solution (sodium phosphate buffer, pH 7.4) with rate constants of approximately 10(4) M-1 s-1, resulting in the generation of NO2-/NO3- and imidazolineoxyls such as 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl (PTI), carboxy-PTI, or carboxymethoxy-PTI. Furthermore, the effects of imidazolineoxyl N-oxides on acetylcholine- or ATP-induced relaxation of the smooth muscle of rabbit aorta were tested. The vasorelaxations were inhibited by all three imidazolineoxyl N-oxides markedly. The inhibitory effects of carboxy-PTIO was almost 2-fold stronger than those of .NO synthesis inhibitors, N omega-nitro-L-arginine and N omega-monomethyl-L-arginine. Generation of EDRF/.NO was identified by reacting the PTIO in aortic strips and quantitating the reaction product with ESR spectroscopy. Thus, it was clarified that imidazolineoxyl N-oxide antagonize EDRF/.NO via a unique radical-radical reaction with .NO.
Acetylcholine↗
Serial changes in atrial and brain natriuretic peptides in patients with acute myocardial infarction treated with early coronary angioplasty.
To examine the role of brain natriuretic peptide (BNP) in acute myocardial infarction (AMI), we measured the plasma concentration of immunoreactive (ir) BNP together with that of atrial natriuretic peptide (ANP) over the 4-week course of AMI in 16 patients treated with early coronary angioplasty. Both the plasma ir-ANP and ir-BNP levels were increased on the first day of the infarction compared with the values in normal subjects. During the clinical course of the infarction, the plasma ir-ANP concentration soon decreased, while the plasma ir-BNP level remained elevated at 2 weeks after the infarction, also exhibiting a high level at 4 weeks. Plasma ir-BNP levels on day 1 or days 14 and 28 were inversely correlated with left ventricular ejection fraction obtained by left ventriculography at the acute or chronic phase, respectively. Plasma ir-BNP concentrations on days 14 and 28 were positively correlated with the maximal myosin light chain I level, an indicator of infarct size. These observations suggest that the plasma ir-BNP level increased to compensate for the ventricular dysfunction associated with the size of the infarct in AMI. BNP may act as a cardiac hormone in AMI, differing somewhat from ANP in its synthetic, secretory, or clearance behavior.
Angioplasty, Balloon, Coronary↗
Stimulation of endothelin-1 release by low density and very low density lipoproteins in cultured human endothelial cells.
To examine the effects of lipoproteins on the secretion of endothelin-1 from endothelial cells, we measured immunoreactive (ir) endothelin-1 release from cultured human umbilical vein endothelial cells in the presence or absence of various concentrations of native low density lipoprotein (LDL), oxidized LDL, and very low density lipoprotein (VLDL). Cultured endothelial cells secreted ir-endothelin-1 into serum-free medium in a time-dependent manner, and the secretion was clearly stimulated following a 15-24-h incubation with 10 micrograms/ml oxidized LDL. The secretion of ir-endothelin-1 increased in a dose-dependent manner after a 24-h incubation with oxidized LDL, while only a high dose of native LDL and VLDL significantly increased ir-endothelin-1 secretion. The release of ir-endothelin-1 stimulated by 20 micrograms/ml oxidized LDL was reproduced by the same concentration of acetylated LDL but not native LDL. These observations indicate that the release of ir-endothelin-1 from endothelial cells is stimulated by lipoproteins, in particular by oxidized LDL, probably through the endothelial scavenger receptor. This increase in ir-endothelin-1 release induced by oxidized LDL may contribute to the development of atherosclerotic vascular lesions.
Cells, Cultured↗
Effect of endothelin receptor antagonist, BQ-123, on Ca2+ signaling in cultured rat mesangial cells.
Endothelin (ET)-1 causes mesangial cell contraction and proliferation. The present study was designed to evaluate the functional ET receptor subtype in cultured rat mesangial cells by measuring intracellular Ca2+ signaling with the use of a newly synthesized ET receptor type A selective antagonist-BQ123. The ET-1, ET-2 and ET-3 increased intracellular Ca2+ level in a dose-dependent manner. BQ-123 suppressed intracellular Ca2+ elevation in response to ET-1 in a dose-dependent manner with its half maximal inhibition value of 28 nM. BQ-123 (10(-6) M) did not affect ET-3 (10(-7) M)-induced Ca2+ response. The peak Ca2+ levels after addition of ET-3 without BQ-123 were similar to those in response to ET-1, ET-2 and ET-3 in the presence of BQ-123. Northern blot analysis showed that cultured mesangial cells expressed both ETA and ETB receptor mRNA. These results suggest that cultured mesangial cells have, at least, two types of functional receptors, one of which is an ETA receptor.
Amino Acid Sequence↗
Stimulation of brain natriuretic peptide release from the heart by thyroid hormone.
This study was designed to examine the involvement of thyroid hormone in the release of brain natriuretic peptide (BNP) from the heart. We measured plasma immunoreactive BNP (ir-BNP) concentrations in patients with untreated hyperthyroidism. We also measured BNP values in experimental rats with hyperthyroidism induced by thyroxine (T4) and in rats with hypothyroidism induced by propylthiouracil (PTU). The in vitro effects of triiodothyronine (T3) and T4 on the release of BNP were examined in newborn rat atrial and ventricular myocytes in primary culture. Plasma BNP levels were increased in hyperthyroid patients compared with normal control subjects. Plasma BNP levels were increased in hyperthyroid rats and decreased in hypothyroid rats compared with euthyroid rats. Plasma BNP level was correlated with serum T4 level in hyperthyroid patients and hyperthyroid rats. A major component of ir-BNP in plasma from hyperthyroid patients was human BNP-32 and that in plasma from hyperthyroid rats was rat BNP-45. T4 and T3 stimulated release of ir-BNP from both cultured atrial and ventricular myocytes in a dose-dependent manner. Plasma BNP concentration is frequently increased in hyperthyroidism, and thyroid hormone may regulate BNP release from both atrial and ventricular myocytes.
Adult↗
Cosecretion of atrial and brain natriuretic peptides stimulated by endothelin-1 from cultured rat atrial and ventricular cardiocytes.
We examined the secretion of immunoreactive (ir) atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) in primary cultures of atrial and ventricular cardiocytes from neonatal rats, and also investigated the stimulatory effect of endothelin-1 (ET-1) on ir-ANP and ir-BNP release from these cells. After 2 days of culture, rat atrial and ventricular cardiocytes secreted both ir-ANP and ir-BNP into serum-free medium in a time-dependent manner. The amount of ir-BNP released per 10(5) ventricular cells was approximately 60% to 70% (1.8 +/- 0.5 pg/h, 2.5 +/- 0.4 pg/2 h, 2.6 +/- 0.4 pg/4 h) of that released from atrial cells (2.8 +/- 0.4 pg/h, 3.5 +/- 0.6 pg/2 h, 4.6 +/- 0.6 pg/4 h), although ir-ANP was secreted almost entirely from atrial cells. ET-1 clearly stimulated secretion of both ir-ANP and ir-BNP in atrial and ventricular cardiocytes. These observations indicate that ir-BNP is cosecreted with ir-ANP not only from atrial cardiocytes, but also from ventricular cardiocytes in the rat, and that ET-1 stimulates the secretion of these natriuretic peptides by a direct mechanism, not through a hemodynamic change.
Animals↗
Effects of maxillomandibular fixation on respiration.
The effects of maxillomandibular fixation (MMF) on respiration were studied by measuring pulmonary function in 27 healthy volunteer subjects and in six post-operative patients who underwent MMF after sagittal split ramus osteotomies. In addition, airflow resistance of the mouth was measured in seven healthy subjects under MMF. In the healthy subjects, the ratio of forced expiratory volume in one second to forced vital capacity and peak expiratory flow rate were reduced by 22.9% and 52.1%, respectively, after application of MMF, indicating the presence of respiratory obstruction, whereas the ratio of forced vital capacity to predicted forced vital capacity, an indicator of restrictive respiratory defects, was not significantly affected. The obstructive type of respiratory defect was found to be the result of increased airflow resistance with MMF. The decrease of forced expiratory volume was greater in all postoperative patients than in the healthy subjects. The results indicate that careful preoperative and postoperative airway management is essential for the safety of patients undergoing MMF for the treatment of oral and maxillofacial conditions.
Adult↗
Effect of heparin on endothelin-1 production by cultured human endothelial cells.
Heparin shows a blood pressure-lowering effect in various hypertensive rat models. This study was designed to examine the effect of heparin on vasoconstrictor endothelin-1 (ET-1) production by cultured human umbilical vein endothelial cells (HUVECs). ET-1 and cyclic GMP levels in the medium were determined by radioimmunoassay. ET-1 mRNA was quantified by densitometric Northern blot analysis. ET-1 was released into the medium in a time-dependent manner, and its release was augmented by thrombin (10 U/ml). Heparin suppressed both basal and thrombin-stimulated ET-1 secretion and its mRNA expression in a dose-dependent manner. Heparin suppressed ET-1 mRNA expression in a time-dependent fashion. Heparin did not suppress both basal and thrombin-stimulated ET-1 production in the presence of NG-monomethyl-L-arginine (L-NMMA) (10(-5) M). The production of cGMP stimulated by thrombin was significantly enhanced by heparin, but not in the presence of L-NMMA (10(-5) M). Heparin may suppress vasoconstrictor ET-1 production mediated by the enhancement of endothelium-derived nitric oxide in HUVECs.
Blotting, Northern↗
Description of proton elastic scattering on 6,7,9,11Li with microscopic effective interaction.
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Journal Article↗
Interaction of PDGF and natriuretic peptides on mesangial cell proliferation and endothelin secretion.
The present study examined the possible interaction of platelet-derived growth factor (PDGF) and atrial or brain natriuretic peptides (ANP and BNP, respectively) on cellular proliferation and secretion of endothelin-1 in cultured rat mesangial cells. PDGF increased cellular proliferation and endothelin-1 secretion. The protein kinase C (PKC) inhibitors, 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine, staurosporine, and PKC inhibitor peptide, inhibited such stimulation. Rat ANP-(1-28) and rat BNP-45 exhibited clearly dose-related inhibition of PDGF-stimulated cellular proliferation and endothelin-1 secretion. This inhibition by ANP and BNP was paralleled by an increase in the cellular level of guanosine 3',5'-cyclic monophosphate (cGMP). Results indicate that PDGF stimulates cellular proliferation and endothelin-1 secretion in cultured rat mesangial cells by a mechanism probably involving activation of PKC and that ANP and BNP inhibit such stimulation through a cGMP-dependent process.
1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗