Search PubMed⌕ Search

Biomedical subjects

Z Ota

Publications and source records attributed to Z Ota.

At least 181 records · Page 10Linked to original sources
PubMed1989

[Complement-mediated solubilization of immune complexes in immune complex nephritis].

In order to examine the ability of complement to solubilize the immune complexes (IC) in vivo, we made acute or chronic serum sickness nephritis in 10 rabbits or 12 rats with injection of BSA as antigen (Ag). Animals were divided into two groups. The 500 mu or 50 mu/week of cobra venom factor (CVF) for rabbits or rats was administered intraperitoneally in one group of animals to reduce the serum complement levels and complement-mediated solubilization of immune complex. On the other hand, the 2 ml or 0.2 ml/week of turpentine oil (TO) was injected intramuscularly in another group of animals to elevate the serum complement levels. The renal biopsy was performed with weekly intervals in each animals, and the specimens were stained for antigen (BSA), antibody (IgG) and C3 by immunofluorescence techniques. The result in this experiments showed the significant difference between TO-, and CVF-treated animals in the degree of disappearance of IC in the kidney lesions. The undetectable amount of IC (especially BSA) was remained in the renal tissue of TO-treated animals. This fact indicated that complement might act to solubilize the IC deposited in the tissue in vivo also.

Animals↗
PubMed1989

Three-dimensional architecture of the mesangial matrix--comparison of the intact and acellular glomerulus.

The three-dimensional ultrastructure of the rat mesangial matrix was studied in acellular rat renal cortex in comparison with intact cortex by scanning electron microscopy (SEM). The mesangial region was covered with fenestrated endothelial cells and was not identified in untreated specimens by SEM. Acellular renal cortex was obtained by perfusion with 4 mM EDTA, 3% Triton X-100, 0.0025% deoxyribonuclease in 1 M NaCl and 4% sodium deoxycholate. Transmission electron microscopy revealed that the glomerular basement membrane (GBM) and mesangial matrix maintained their respective shape and did not collapse even after removal of the cellular components. By SEM, the mesangial matrix appeared as fenestrated septa with oval or round stomata between the glomerular capillaries. The diameter of the stomata was 601 +/- 290 nm. The diameter of the fibrils forming the stomata was 177 +/- 80 nm. These fenestrated structures of the mesangial matrix appear to be useful in supporting glomerular tufts, in stretching and retracting mesangial cells and in passing macromolecules from the capillary lumen into the mesangium.

Animals↗
PubMed1989

[A case of nephrotic syndrome associated with pulmonary infarction and renal vein thrombosis. (A review of literature)].

A case of nephrotic syndrome found by pulmonary infarction associated with renal vein thrombosis was reported. The renal biopsy showed the presence of membranous glomerulonephritis. The patient had the increase of serum level of the coagulation factor II, V, fibrinogen and FDP, and the level of urine FDP. These laboratory data suggested that the hyper coagulation state of his blood caused by nephrotic state, induced his multiple thromboembolism. We surveyed 47 case report abstracts of nephrotic syndrome patients having thromboembolism on the Japanese Journal of Nephrology published from 1974 to 1986. The histopathology of their renal biopsies showed the high incidence of membranous glomerulonephritis, followed by minimal change nephrotic syndrome and focal glomerular sclerosis. Renal vein thrombosis was the most common thromboembolism in the reports, followed by thrombosis of cerebral vessels, peripheral vessels and pulmonary artery. Some patients died of pulmonary infarction or myocardial infarction. These data showed that we must keep in mind of the possibility of thromboembolism in the treatment of nephrotic syndrome.

Glomerulonephritis, Membranous↗
PubMed1989

Effect of daily energy expenditure on the creatinine clearance and daily urinary protein excretion of patients with mesangial proliferative glomerulonephritis.

In the present study, the relationships among daily energy expenditure, renal function (creatinine clearance, Ccr), and daily urinary protein excretion were examined. In total, 104 adult patients (from 9 renal clinics in Japan) with primary chronic glomerulonephritis were fitted with a portable calorie counter for about two weeks to estimate their daily energy expenditure. On two separate days when the energy expenditure was expected to be contrastingly different, urine collection and blood sampling were performed, and the Ccr and daily urinary protein excretion were determined. Multiple regression analysis of Ccr clearly demonstrated a significant correlation between its acceleration and increase in the daily protein intake or protein excretion. In mesangial proliferative glomerulonephritis showing a constant level of protein intake, the enhancement of Ccr revealed a significant inverse relation to the increase in daily energy expenditure (%BMR). It was demonstrated statistically that a daily energy expenditure exceeding 150 %BMR slowed the Ccr down. This limit was almost the same as the level in healthy adults living in urban cities of Japan. The urinary protein excretion was significantly correlated with the daily protein intake. These results should be taken into consideration in prescribing for each individual patient an allowable degree of labor or any other activity and an adequate dietary regimen, and also in evaluating the efficacy of a drug for glomerulonephritis.

Adolescent↗
PubMed1988

Effect of atrial natriuretic peptide on acetylcholine-induced release of corticotropin-releasing factor from rat hypothalamus in vitro.

Effect of rat atrial natriuretic peptide (rANP) on acetylcholine-induced release of corticotropin-releasing factor (CRF) from the rat hypothalamus was studied in vitro using perifusion method. Perifused acetylcholine at 100 and 1000 ng/ml evoked significant CRF release, whereas norepinephrine at 10, 100 and 1000 ng/ml did not show a definite effect on CRF release. Continuous administration of alpha-rANP(1-28) (20ng/ml) inhibited the acetylcholine (100ng/ml)-induced CRF release. It is likely that ANP is involved in the regulation of CRF release.

Acetylcholine↗
PubMed1988

Central catecholaminergic control of ACTH secretion.

Plasma adrenocorticotropic hormone (ACTH) has been measured after an intra-third ventricular administration of noradrenaline, an adrenergic agonist or an adrenergic antagonist. Centrally administered noradrenaline caused a significant increase in ACTH secretion. The alpha-agonist phenylephrine also increased the ACTH level. However, neither the alpha-antagonist phentolamine nor beta-agonist isoproterenol affected the ACTH level. The beta-antagonist propranolol evoked a significant elevation in ACTH. Passive immunoneutralization was examined with anti-rat corticotropin-releasing factor (CRF) rabbit serum, anti-arginine vasopressin (AVP) rabbit serum and normal rabbit serum (NRS) on the intra-third ventricular noradrenaline-induced ACTH secretion to study the involvement of endogenous CRF. An intra-third ventricular administration of noradrenaline caused a significant increase of ACTH levels in NRS-injected rats and anti-AVP-injected rats, whereas an i.v. anti-rat CRF injection significantly reduced the intra-third ventricular noradrenaline-induced ACTH secretion. These results suggest that central catecholamine stimulated ACTH secretion via the alpha-adrenergic mechanism and that endogenous CRF is at least partly involved in the noradrenaline-induced ACTH secretion.

Adrenocorticotropic Hormone↗
PubMed1988

Corticotropin-releasing hormone and pituitary-adrenocortical responses in chronically stressed rats.

Brain corticotropin-releasing hormone (CRH) concentration and pituitary adreno-cortical responses were examined in chronically stressed rats: body restraint stress (6 h/day) for 4 or 5 weeks. Stressed rats showed a reduction in weight gain. CRH concentration in the median eminence and the rest of the hypothalamus were not different between control and chronically immobilized rats. The anterior pituitary adenocorticotropic hormone (ACTH) concentration was elevated in chronically stressed rats, whereas plasma ACTH and corticosterone levels did not differ from the control values. The median eminence CRH concentration was reduced to the same extent at 5 min after onset of ether exposure (1 min) in chronically immobilized rats and controls. However, plasma ACTH and corticosterone showed greater responses to ether stress in chronically immobilized rats than in control rats. Plasma ACTH and corticosterone responses to exogenous CRH were not different between control and chronically immobilized rats, while the response to arginine vasopressin (AVP) was significantly greater in chronically immobilized rats. These results suggest that chronic stress caused an increase in the ACTH-secreting mechanism and that pituitary hypersensitivity to vasopressin might at least be partly responsible for this.

Adrenocorticotropic Hormone↗
PubMed1988

Localization of receptors for atrial natriuretic polypeptide (ANP) in the glomerulus: in vitro electron microscopic autoradiographical investigation using 125I-labeled ANP.

The localization of receptors for atrial natriuretic polypeptide (ANP) in the glomerulus of the rat was studied by electron microscopic autoradiography using 125I-labeled ANP. A total of 1,134 silver grains counted in 30 glomeruli were distributed as follows: processes of the podocytes (36.4%), cell bodies of the podocytes (14.8%), basement membrane (12.3%), endothelial cells (6.3%), mesangial cells (7.7%) and others, for example the vascular spaces (22.5%). This finding indicates that ANP binding sites are mainly localized on the foot processes of the podocytes in the glomerulus.

Animals↗
PubMed1988

Involvement of prostaglandin E2, cAMP, and vasopressin in lithium-induced polyuria.

The involvement of prostaglandin E2 (PGE2), adenosine 3',5'-cyclic monophosphate (cAMP), and vasopressin in lithium-induced polyuria was investigated in rats. Administration of LiCl (4 mmol/kg body wt) for 7 days induced a marked polyuria with a significant excretion of urinary PGE2. Administration of indomethacin (IND, 5 mg/kg body wt) for 4 days to lithium-induced diabetes insipidus (LiDI) rats diminished urine volume by 80% and urinary PGE2 by 85%. The in vitro data of the intact rat kidney showed that lithium stimulated arginine vasopressin (AVP)-induced PGE2 production and suggested that PGE2 suppressed cAMP synthesis in rat renal medulla. The AVP-induced PGE2 synthesis was greater and the AVP-stimulated cAMP production lower in the LiDI rat kidney in vitro. Interference of the vasopressin-associated cAMP system and the increased PGE2 synthesis in the kidney may be involved in the development of LiDI. The reduced cAMP production in the LiDI rat kidney might be partly due to the increased PGE2 synthesis. In LiDI rats plasma vasopressin increased, whereas AVP concentration in the hypothalamus and the neurohypophysis significantly decreased. It is postulated that lithium stimulates vasopressin release from the central nervous system and that elevated plasma vasopressin potentiates PGE2 production in the kidney synergistically with lithium.

1-Methyl-3-isobutylxanthine↗
PubMed1988

Mechanism of hematuria. II. A scanning electron microscopic demonstration of the passage of blood cells through a glomerular capillary wall in rabbit Masugi nephritis.

A model of hematuria was established in rabbits. An accelerated form of unilateral Masugi nephritis was induced in 10 New Zealand white rabbits by an intravenous injection of duck antirabbit kidney serum and by ligating the left renal artery immediately after the injection of the antibody. All 10 rabbits became hematuric 1-2 weeks after the injection of the antibody and red blood cell (RBC) casts were found in the urinary sediment of all these animals. An ultrastructural examination of renal glomeruli by transmission electron microscopy revealed the transcapillary passage of polymorphonuclear leukocytes through the gaps of the glomerular basement membrane (GBM). RBC were found in the urinary space in 50% of the glomeruli observed by scanning electron microscopy (SEM) and the passage of leukocytes and RBCs through the glomerular capillary wall was also observed. Gaps in the GBM became clearer after the removal of cellular components by detergents. In control rabbits, no RBCs could be observed in the urinary space, and isolated GBM were intact by SEM. These data further support the hypothesis that in rabbit Masugi nephritis hematuria is a result of the passage of RBCs through gaps in the GBM.

Animals↗
PubMed1988

Human corticotropin-releasing factor plus lysine vasopressin test during glucocorticoid therapy.

1.0 micrograms/kg body wt human corticotropin-releasing factor (hCRF) and 0.005 IU/kg body wt lysine vasopressin (LVP) were administered in a bolus dose to patients receiving daily or alternate-day glucocorticoid therapy. In normal subjects with this hCRF-LVP test, the plasma ACTH increment was significantly greater (approximately 2.5-fold) 15 min after injection than under the CRF test. In patients receiving daily glucocorticoid therapy (greater than 15 mg prednisolone or an equivalent daily dose), the plasma ACTH and cortisol responses to hCRF-LVP were suppressed 2 wk to 1 mo after the beginning of glucocorticoid administration but partially improved at 2-10 mo, and was markedly suppressed several years later. On the other hand, in patients receiving alternate-day glucocorticoid therapy, the plasma ACTH response was normal at 2 wk, normal or higher at 1-3 mo, and normal after 4 mo. A normal plasma cortisol response was observed throughout the test period in patients receiving alternate-day therapy after pulse therapy, whereas plasma cortisol response was gradually improved in patients receiving alternate-day therapy after several months of daily therapy.

Adolescent↗
PubMed1988

Five patients with painless thyroiditis simultaneously developed in a nursery school.

Painless (silent) thyroiditis (PT) occurred simultaneously in 1 male and 4 females aged 21 to 52 years working at a nursery school. Clinical symptoms did not include goiter, or pain or tenderness of the neck in any of the patients but were characterized by edema of the lower legs as well as palpitation and loss of body weight as observed in subacute thyroiditis. General blood analysis showed that all patients were negative for C-reactive protein (CRP) and 3 had mild impairment of liver function. Examination of thyroid function suggested transient thyrotoxicosis accompanied by a marked reduction in radioactive iodine uptake (RAIU), but antithyroglobulin hemagglutination antibody (TGHA) and antithyroid microsomal hemagglutination antibody (MCHA) were negative in all patients. Examination of various viral antibodies showed no significant changes in their titers. Thyrotoxicosis was transient and disappeared without treatment or by glucocorticoid administration. Our results suggested that PT observed in this study was caused by some environmental factor. The possibility of an unidentified virus as a factor cannot be ruled out.

Adult↗
PubMed1988

Effects of lithium on the hypothalamo-pituitary-adrenal axis.

The effect of lithium on the hypothalamo-pituitary-adrenal axis was studied in vivo and in vitro. The levels of plasma vasopressin, ACTH and corticosterone increased after the administration of lithium (LiCl 4 mmol/kg BW, 11 days) in rats, while the tissue vasopressin concentration in the median eminence, the rest of the hypothalamus and the posterior pituitary was decreased. The CRF concentration in the posterior pituitary increased markedly, but it did not change significantly in the median eminence or the rest of the hypothalamus. The elevated plasma ACTH level might be at least partly due to the increased vasopression secretion. Lithium stimulated ACTH secretion per se and also enhanced vasopressin-induced ACTH secretion in cultured pituitary cells and in half pituitary incubations, while it did not affect CRF-induced ACTH secretion. Lithium inhibited CRF-induced cAMP accumulation in half pituitary incubations, while lithium and vasopressin did not affect cAMP accumulation per se or even when administered together. The results suggest that lithium-induced ACTH release is via a cAMP-independent mechanism. Thus, it is possible that lithium stimulates ACTH release by acting directly on the corticotroph, stimulating vasopressin release and potentiating vasopressin-induced ACTH release.

Adrenocorticotropic Hormone↗
PubMed1988

Mild adrenal 3 beta-hydroxysteroid dehydrogenase deficiency with hyperaldosteronism.

The patient was admitted to our hospital at 19 and again at 22-yr of age for hirsutism and hypertension. Her baseline and ACTH-stimulated plasma 17-hydroxy pregnenolone, dehydroepiandrosterone and dehydroepiandrosterone sulfate were increased whereas plasma 17-hydroxy progesterone and androstenedione were normal and responded poorly to ACTH. Plasma deoxycorticosterone, corticosterone and cortisol baseline levels were normal, and they responded normally to ACTH. The plasma aldosterone concentration (PAC) was always high and responded well to ACTH, angiotensin III and furosemide-upright stimulation. However, plasma renin activity (PRA) was normal or slightly high, and responded normally to furosemide-upright stimulation and fluorohydrocortisone suppression. Dexamethasone (2 mg/day) for 1-2 weeks suppressed the androgens, cortisol and corticosterone levels. PRA and PAC were suppressed temporally, but PRA returned to normal and PAC to be a high level after 2 weeks of dexamethasone administration. Blood pressure was also reduced temporally but returned to a high level after 2 weeks of dexamethasone. These results indicate that primary aldosteronism and dexamethasone-suppressible hyperaldosteronism were not likely to be present, and unknown aldosterone stimulating factors which potentiated the action of endogenous angiotensin II or ACTH might be responsible for the hyperaldosteronism in this patient. We conclude that this patient had a mild and non-salt losing 3 beta-HSD deficiency in the zona reticularis with normal fasciculata and high glomerulosa function.

3-Hydroxysteroid Dehydrogenases↗
PubMed1988

In vitro release of immunoreactive atrial natriuretic peptide from the rat atria.

In vitro release of atrial natriuretic peptide (ANP) from atria was examined by ANP radioimmunoassay. Isolated right rat atria were incubated in Krebs-Ringer bicarbonate buffer, and test substances were added to the incubation medium. The fluid was assayed for rat ANP by a radioimmunoassay method recently developed in our laboratory. We produced an antiserum to human ANP(99-216) (alpha-hANP(1-28)) which showed a good cross-reactivity of 63% with rat ANP(99-126) (alpha-rANP(1-28)) and was useful for measuring rat ANP concentrations of the medium. Application of the medium to a reverse phase high performance liquid chromatography (HPLC) system resulted in a single peak of immunoreactive rat ANP corresponding to a small molecular weight synthetic rat ANP of 28 amino acid residues. Catecholamines (epinephrine, norepinephrine and isoproterenol) reduced the basal secretion of ANP, whereas acetylcholine stimulated the release of ANP. Forskolin and dibutyryl cyclic AMP did not affect the release of ANP. These results suggest the possibility that the regulation of ANP release may be partially associated with adrenergic and cholinergic mechanisms.

Acetylcholine↗
PubMed1988

Changes in the molecular sieve of the glomerular basement membrane of rats with chronic serum sickness.

In order to explore the pathogenic mechanism of proteinuria in glomerulonephritis, ultrastructural changes of the glomerular basement membrane were investigated in rats with chronic serum sickness induced by repeated intravenous injections of bovine serum albumin (experimental rats). Rats injected with saline served as controls. The animals were sacrificed and examined 13 weeks after treatment, when the mean urinary protein of experimental animals reached 206 mg/24h/100g body weight. Enhanced transcapillary passage of anionic ferritin was observed in experimental rats. Purified glomerular basement membranes of control and experimental rats were examined by electron microscopy after negative staining. The glomerular basement membrane of experimental rats had enlarged pores. The results suggest that an increase in the radius of glomerular pores may be responsible for proteinuria in glomerulonephritis.

Animals↗