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Biomedical subjects

M Endoh

Publications and source records attributed to M Endoh.

At least 397 records · Page 22Linked to original sources
PubMed1984

Focal segmental glomerulosclerosis associated with a pheochromocytoma.

A 22-year-old male patient with focal segmental glomerulosclerosis(FSGS) associated with a pheochromocytoma is reported. Immunofluorescence study of the kidney biopsy specimen demonstrated segmental depositions of IgM, C3 and fibrinogen. Alteration of glomerular basement membrane(GBM) with fibrin strands and platelet aggregates was observed by electron microscopic examination. Administration of prednisolone had no effect on massive proteinuria, but surgical removal of the tumor promptly reduced proteinuria. It was suggested that FSGS can develop in patients with pheochromocytomas, and local hypercoagulation might be responsible for the development of this lesion.

Adrenal Gland Neoplasms↗
PubMed1984

A case of Behçet's disease associated with membranous nephropathy.

A 35-year-old female patient with Behçet's disease associated with nephrotic syndrome is described. Renal biopsy specimens revealed typical features of membranous nephropathy in light microscopical, electron microscopical and immunofluorescent microscopical examinations. Circulating immune complexes (IC) phagocytized by polymorphonuclear leukocytes (PMN) in this patient were significantly increased compared with those in healthy adults. Recurrent oral aphthous ulcers had persisted for 14 years. In the course of Behçet's disease, nephrotic syndrome due to membranous nephropathy was observed. Depositions of IgA, IgM, C3 and C4 were observed in the subcutaneous arteriolar walls by immunofluorescence. It is suggested that the pathogenesis of Behçet's disease and membranous nephropathy might be due to a deposition of circulating immune complexes in various types of vascular vessels in this patient.

Adult↗
PubMed1983

Relationship between relaxation and cyclic GMP formation caused by nicorandil in canine mesenteric artery.

In the isolated canine mesenteric artery relaxation caused by nicorandil [N-(2-hydroxyethyl)nicotinamide nitrate ester; SG-75] in the presence of noradrenaline was accompanied by a concomitant elevation of cGMP level, whilst the cAMP level was not changed by the drug. The relaxation and cGMP level after the administration of nicorandil showed a good correlation. In this respect nicorandil is very similar to nitrogen oxide-containing vasodilators.

Animals↗
PubMed1983

Impaired solubilization of glomerular immune deposits by sera from patients with IgA nephropathy.

A study of the solubilization of glomerular immune deposits by sera from patients with IgA nephropathy is described. Renal biopsy specimens were obtained from patients with IgA nephropathy and other glomerular diseases. These specimens were incubated with fresh and heated sera from the same patients and healthy adults at 37 degrees C for one hour in plastic tubes. The sections were stained with fluorescein isothiocyanate (FITC)-labeled heavy chain specific anti-human IgA antiserum and then examined with a fluorescent microscope. It was shown that the solubilization of glomerular immune deposits by sera from patients with IgA nephropathy was significantly less than that by sera from healthy adults. It is possible that impaired solubilization of immune complexes in vivo could lead to the accumulation of glomerular immune deposits in patients with IgA nephropathy.

Antigen-Antibody Complex↗
PubMed1983

In vitro induction of altered response of rat atria to acetylcholine with histamine-sensitizing factor of Bordetella pertussis.

Purified histamine-sensitizing factor (HSF) of Bordetella pertussis induced in vitro an alteration in the pharmacologic response of rat atria to acetylcholine. Spontaneously beating atrial preparations isolated from rats were exposed to HSF at a concentration of 50 ng/ml at 37 C for 30 min to 4 hr and washed with Krebs-Ringer solution, and then tested at 1-hr intervals up to 28 hr during incubation for their responses to epinephrine and acetylcholine. At 13 hr after exposure to HSF, irrespective of the exposure period, the HSF-treated atria, in which positive-inotropic action of epinephrine was manifested, depressed the negative-inotropic response to acetylcholine. The activity of HSF was neutralized by anti-HSF serum only in the first 3 hr exposure. Only 1.8% of the added 125I-labeled HSF bound "specifically" to one pair of atria for the manifestation of the altered response.

Acetylcholine↗
PubMed1983

Increase of peripheral blood B cells with Fc receptor for IgA in patients with IgA nephropathy.

A B-cell subset with Fc receptors for IgA (B alpha cells) has been observed in human peripheral blood. To investigate aberrations of B cells in a diseased state, the percentages of B alpha cells were enumerated in peripheral blood from patients with IgA nephropathy, which is characterized by preponderant deposition of IgA-dominant immune complexes in the glomerular mesangial area. The present study showed a significant increase in B alpha cells in peripheral blood from patients with IgA nephropathy but not in those with chronic proliferative glomerulonephritis without mesangial IgA deposition. Most Fc alpha R-bearing cells were observed in surface IgA bearing lymphocytes. No linear correlation was observed between the levels of serum IgA and the percentages of B alpha cells. The addition of aggregated IgA to cultures did not induce Fc alpha R-bearing B cells in vitro. It is postulated that B alpha cells might have some pathogenetic role in the development of IgA nephropathy and that some antigenic stimuli might play a role in the increase of peripheral blood B alpha cells in patients with IgA nephropathy.

B-Lymphocytes↗
PubMed1983

Immunopathological similarities between IgA nephropathy and Henoch-Schoenlein purpura (HSP) nephritis.

A study on the immunopathological similarities between IgA nephropathy and Henoch-Schoenlein purpura (HSP) nephritis is described. Various examinations were performed as follows. (1) Pathological studies: light microscopic findings and immunofluorescent staining; (2) Measurement of the levels of IgA in pharyngeal washings and sera, and those of IgA quantitated by radial immunodiffusion; (3) Elution studies: renal biopsy specimens obtained from patients with IgA nephropathy and HSP nephritis were treated with citrate buffer (pH 3.2) and the "eluate" was neutralized by sodium hydroxide. The "eluate" was then applied to the acid-treated sections obtained from the same and other patients with IgA nephropathy as well as sections from patients with HSP nephritis and other glomerular diseases. The sections were stained with FITC-conjugated heavy chain specific antihuman IgA antisera and then examined with a fluorescent microscope. There were no differences in pathological findings of IgA nephropathy and HSP nephritis in the light microscopic and immunofluorescent examinations. The levels of IgA in pharyngeal washings and sera were significantly increased in patients with both diseases. IgA antibodies deposited in kidneys from patients with HSP nephritis crossreacted with kidneys from some patients with IgA nephropathy, and vice versa. However, antibodies from patients with IgA nephropathy and HSP nephritis did not react with normal glomeruli or other nephritic glomeruli. It is concluded that there are some immunopathological similarities between IgA nephropathy and HSP nephritis.

Adolescent↗
PubMed1983

Stress-mediated effect of metoclopramide on cortisol secretion in man.

Five healthy adult men were given metoclopramide (10 and 20 mg) iv, and in repeated tests almost always developed transient restlessness lasting from 10-30 min. The effects of L-dopa and dexamethasone on metoclopramide-induced increases in cortisol concentration were determined. These response values were compared with those of a control. After an injection of 10 mg metoclopramide, the cortisol level increased significantly only at 40 min; the ACTH level did not change. The cortisol rise was suppressed by dexamethasone pretreatment. Pretreatment with 0.5 g L-dopa resulted in a decrease in the PRL level from -20 min to 20 min, and the increase in cortisol seen at 40 min was cancelled. The ACTH level did not change. After injecting 20 mg metoclopramide, the ACTH level increased significantly from 20 min to 60 min and the cortisol level showed a significant increase from 20 min to 120 min. Pretreatment with dexamethasone resulted in a decrease in these hormones. The L-dopa pretreatment did not reduce even the rise in the PRL level which resulted from the administration of 20 mg metoclopramide. These findings suggest that the ACTH and cortisol response to metoclopramide is a stress-mediated effect. Plasma cortisol responses to 20 mg metoclopramide and insulin-induced hypoglycemia were studied and compared in seven volunteers and found to be similar.

Adrenocorticotropic Hormone↗
PubMed1983

Adrenocorticotropin-mediated effect of metoclopramide on plasma aldosterone in man.

Five healthy adult men were given metoclopramide (10 and 20 mg) iv and the effects of L-dopa and dexamethasone on metoclopramide-induced increases in plasma aldosterone concentration were determined. Plasma PRL, ACTH, and cortisol levels were also measured and the results reported in a previous study. After an injection of 10 mg metoclopramide, aldosterone levels increased significantly. The aldosterone rise was inhibited by L-dopa, but not by dexamethasone. After injecting 20 mg metoclopramide, aldosterone levels increased significantly vs. both the control and the basal level. The aldosterone increase was not inhibited by L-dopa pretreatment, whereas pretreatment with dexamethasone did suppress it. The data suggest that metoclopramide increased aldosterone secretion through an ACTH-dependent (stress mediated) effect in addition to its antidopaminergic adrenal action, simultaneously. There were no significant differences between the ACTH-dependent and dopamine antagonist-mediated aldosterone increases in either the 10- or 20-mg tests. However, the ACTH-dependent aldosterone increase was statistically greater in the 20-mg test than in the 10-mg test, whereas there was only a slight and not statistically significant difference in the dopamine antagonist-mediated aldosterone increase between the tests. This means that the ACTH-dependent component of the aldosterone secretion is affected by the doubling of the metoclopramide dose, whereas the dopamine antagonist-mediated component is not.

Adrenocorticotropic Hormone↗
PubMed1983

Pharmacologic effects of metformin in relation to its disposition in alloxan diabetic rats.

The purpose of this investigation is to elucidate the relationship between the time course of pharmacologic effects and drug disposition after administration of metformin, an oral antidiabetic drug of biguanides. Alloxan diabetic rats and normal rats were used in the experiments. After administration of metformin, plasma glucose levels, blood pyruvate levels, blood lactate levels, plasma pancreatic glucagon immunoreactivity (pancreatic GI) and plasma gut glucagon like immunoreactivity (gut GLI) were determined as well as serum concentrations of metformin. In alloxan diabetic rats, gut GLI levels were significantly correlated to the logarithm of tissue metformin levels, calculated from serum metformin levels. The blood lactate, pyruvate and plasma glucose levels were also linearly related to gut GLI levels, after metformin administration. It was also clarified that metformin did not inhibit the intestinal absorption of glucose and that metformin presumably inhibited the hepatic gluconeogenesis. It is reasonable to consider that the effect of metformin on the gut GLI level is the primal effect, and that other pharmacologic effects such as plasma glucose lowering, blood lactate and pyruvate increasing effects are the consequences of the primal effect, at least in alloxan diabetic rats. While in normal rats, plasma gut GLI levels were not significantly related to metformin tissue levels, however, plasma glucose levels were considerably correlated with the logarithm of the plasma or tissue metformin levels. These results indicated that the effect of gut GLI was entirely masked by endogeneous insulin, which might be secreted by metformin administration.

Administration, Oral↗
PubMed1983

Differential effects of 8-bromo-cyclic GMP on the basal contractile force and beta-adrenoceptor-mediated positive inotropic action in the canine atrium.

8-Bromo-cyclic GMP caused a negative inotropic action on the canine atrial muscle, whilst it did not affect the positive inotropic action of phenylephrine mediated via beta-adrenoceptors. These findings are in line with the hypothesis that the muscarinic receptor stimulation may exert functional changes in the heart via two different intracellular biochemical processes: one involving cyclic AMP and the other involving cyclic GMP. 8-Bromo-cyclic GMP mimics the latter but not the former mechanism in canine atria.

Adrenergic beta-Agonists↗