PubMed Health⌕ Search

Biomedical subjects

M Tóth

Publications and source records attributed to M Tóth.

At least 127 records · Page 7Linked to original sources

Relationship between exchangeable body sodium and urinary 6-keto-prostaglandin F1 alpha excretion in normal man.

The renal prostaglandins are involved in the regulation of sodium balance. In the present study exchangeable body sodium (NaE) and the urinary excretion of the stable metabolite of prostacyclin, 6-keto-prostaglandin F1 alpha (6-k-PGF1 alpha) were determined simultaneously in 10 hospitalized healthy individuals. NaE was 1461 +/- 107 mmol/m2 body surface area, or 98.5 +/- 6.9% when expressed as percent of the normal value assessed on the basis of measurements in 54 control subjects. The excretion of 6-k-PGF1 alpha amounted to 68.3 +/- 39.2 ng/4 hr. Statistical evaluation revealed significant correlation between NaE and PGF1 alpha excretion (r = 0.642; p less than 0.05) and between the serum Na concentration and the urinary excretion of 6-k-PGF1 alpha (r = 0.865; p less than 0.001). The obtained results indicate that urinary 6-k-PGF1 alpha excretion, hence the renal synthesis of prostacyclin, are regulated, among other factors, by body sodium stores. The increased production of prostacyclin with expanding sodium space might be regarded as a compensatory response contributing to the renal elimination of excess sodium from the body. The signal to this response could be the serum Na concentration.

6-Ketoprostaglandin F1 alpha↗

[The role of exchangeable sodium content of the body in cases of hypertension of various etiology].

Measurement of exchangeable sodium by isotope dilution is a relatively simple, reliable method for the determination of body sodium contents, which can be used in the clinical practice without significant health hazard to the patient. When computed to body surface area, the values for exchangeable sodium can be compared in patients of different body build. Exchangeable sodium may be variably increased in different clinical conditions associated with hypertension, thus increased sodium contents of the body is of major importance in the pathogenesis of hypertension caused by all forms of mineralocorticoid excess, and in the majority of patients with chronic renal insufficiency. In several endocrine disorders, e. g., acromegaly, hypothyroidism, increased sodium space does not play any significant part in the pathogenesis of hypertension. In diabetes mellitus, exchangeable sodium may be increased already prior to the development of hypertension, however it is still a matter of debate whether this abnormality is involved in the pathogenesis of hypertension in these patients. It seems now beyond any doubt that body sodium is normal in patients with essential hypertension, including those with the low renin form of the disease; nevertheless, some data indicate that blood pressure may be volume dependent in elderly patients with essential hypertension.

Diabetes Mellitus, Type 1↗

[Malignant histiocytosis associated with chronic hepatitis].

A case of malignant histiocytosis successfully treated with splenectomy and chemotherapy is presented. 33 months after surgery the patient's overall condition is satisfactory. The result is attributed to the fact, that in the time of the operation there was no systemic proliferation. The concomitantly present chronic viral hepatitis was worsened by the treatment.

Adult↗

The possible role of tear fluid thyroxine in keratoconus development.

The normal thyroxine level in tears was found to be two orders of magnitude lower than in serum. In thyroxine function tests, keratoconus patients were found to be hypothyreotic, euthyreotic or hyperthyreotic. However, independently of their thyroid function, the tear thyroxine levels of keratoconus patients were 2-50 times higher than that of subjects free of ocular pathology. Tear thyroxine levels were higher during the progression of keratoconus and declined once corneal curvature reached a new steady value.

Adolescent↗

Effects of carbachol and (-)-N6-phenylisopropyladenosine on myocardial inositol phosphate content and force of contraction.

1. The effects of carbachol and the A1-adenosine receptor agonist (-)-N6-phenylisopropyladenosine (PIA) on force of contraction and inositol lipid metabolism were studied in electrically driven left auricles and papillary muscles isolated from guinea-pig hearts. Both carbachol and PIA (0.01-10 microM) had concentration-dependent negative inotropic effects in auricles. In papillary muscles PIA had no inotropic effect. Carbachol also had no inotropic effect at low concentrations (0.01-1 microM) but at 10-100 microM it exerted a slight positive inotropic effect. 2. In auricles and papillary muscles both carbachol and PIA concentration-dependently increased inositol trisphosphate (IP3; significant at 1 microM). Accordingly phosphatidylinositol bisphosphate (PIP2), the precursor of IP3, was reduced. All effects of carbachol and PIA were antagonized by atropine (10 microM) and 1,3-dipropyl-8-cyclopentylxanthine (DPCPX; 20 microM) respectively, indicating receptor-mediated effects. 3. In auricles the negative inotropic effects of carbachol and PIA preceded the increase in IP3. 4. In papillary muscles the increase in IP3 preceded the slight positive inotropic effect of carbachol, indicating that the M-cholinoceptor-mediated increase in IP3 and force of contraction may be related. However, PIA showed a comparable increase in IP3 but no inotropic effect, indicating a dissociation between those parameters. 5. In conclusion, in previous studies a close relation between increases in IP3 and force of contraction has been shown after alpha 1-adrenoceptor stimulation. The present study with carbachol supports this view. However, the present data for PIA could not show such a close relationship, questioning the role of IP3 as an endogenous regulator of force of contraction.

Animals↗

Luteinizing hormone but not endothelin can induce a calcium signal in the chicken granulosa cell.

Using the fluorescent calcium-indicator Indo-1 we demonstrated a rapid transient increase of cytosolic calcium level in dispersed chicken granulosa cells in response to 10-100 ng/ml ovine luteinizing hormone (LH). The magnitude of the signal was dose-dependent, it lasted for about 30 seconds and could be provoked even when the extracellular calcium had been chelated by EGTA. A high, 100 ng/ml concentration of LH abolished completely the responsiveness of these cells to a second exposure to the agonist. We conclude, that LH can mobilize calcium ions from internal store(s) via a desenzitizable mechanism. Finally, endothelin--a vasoactive peptide with Ca2(+)-mobilizing activity in glomerulosa cells--was shown to have no effect on the concentration of cytosolic Ca2+ in chicken granulosa cells.

Animals↗

[The significance of Campylobacter pylori infection in gastroenterologic and diabetic practice].

The presence of Campylobacter pylori was investigated in gastric antral biopsy specimens. In 50 consecutive patients undergoing upper gastrointestinal tract endoscopy microbiological cultures, histological examination and rapid urease test were parallel performed, and a 92 per cent sensitivity and 100 per cent specificity of rapid and cheap urease test were determined. Afterwards--in a prospective study--311 patients were examined for C. p. by the rapid urease test only. C. p. was detected in 92 per cent of duodenal ulcer patients, in 52 per cent of patients with gastric ulcer, in 67 per cent of non-ulcer dyspepsia, in 62 per cent of mixed diabetic patient material, and in 21 per cent only of asymptomatic volunteers. It has been found by the authors, that the rate of C. p. infection increased parallel with the continuance of diabetes and did not follow the increasing with age as in the general population. This is the first observation in the world literature concerning the correlation between C. p. and diabetes mellitus. Very close, significant correlation has been found between C. p. infection and chronic active gastritis. C. p. may play an important role in the recurrences of duodenal ulcer and in the pathogenesis of non-ulcer and diabetic dyspepsia. Further studies are planned to the correct evaluation of pathogeneity of Campylobacter pylori.

Campylobacter Infections↗

[Regression of a pituitary tumor, associated with primary hyperthyroidism, under the effect of 1-thyroxine].

The authors report on a successful medical treatment of a 36-year-old woman who had hypothyroidism and pituitary adenoma. Primary hypothyroidism was evidenced by decreased serum thyroxine (23 nmol/l; 1,77 micrograms/dl) and increased plasma thyroid-stimulating hormone (TSH) levels (108 mU/l). Pituitary mass with suprasellar expansion (1 cm in diameter) was proven by computed tomography (CT). The patient had been treated conventionally with 1-thyroxine and this medication was continued during a 1-year follow-up. Not only did she become symptom-free but control CT scanning revealed a large reduction of tumor size and the disappearance of suprasellar expansion.

Adult↗

The relation between thromboxane and prostaglandin synthesis in human decidua tissue: a comparison of eicosanoid synthesis in minced tissue with that in a cell-free preparation.

Radiotracer studies and radioimmunoassay measurements demonstrate that minced tissues of human decidua produce chiefly thromboxane B2 (TxB2) (70% of total eicosanoids) and small amounts of prostaglandin F2 alpha (PGF2 alpha) (13%) PGD2 (8%), 6-keto-PGF1 alpha (5%) and PGE2 (4%). Inhibition of thromboxane synthesis with a specific inhibitor (OKY-1581: sodium (E)-3-[4(-3-pyridylmethyl)-phenyl]-2-methyl propenoate) increased prostaglandin formation in general, with the main product being PGF2 alpha (38%), a nonenzymic derivative of PGH2. Crude particulate fractions prepared from the same tissue synthesized two major products from [3H]arachidonate, TxB2 and 6-keto-PGF1 alpha (54 and 30%, respectively) and some PGF2 alpha and PGE2 (8-8%). However, in the presence of reduced glutathione (GSH), PGE2 became the main product (81%) (TxB2, 15%; PGF2 alpha, 2%; and 6-keto-PGF1 alpha, 2%). Half-maximal stimulation of PGE2 synthesis occurred at 46 microM GSH. The GSH concentration of tissue samples was found to be 110 +/- 30 microM. We conclude that human first trimester decidua cells possess the key enzymes of prostaglandin and thromboxane synthesis. Apparently, the production of these compounds is controlled by a specific mechanism in the tissue, which keeps PGE and prostacyclin synthesis in a reversibly suppressed state, whereas the formation of thromboxane is relatively stimulated.

6-Ketoprostaglandin F1 alpha↗

Evidence for alpha 1-adrenoceptor-mediated increase of inositol trisphosphate in the human heart.

In human-isolated ventricular myocardium the alpha 1-adrenoceptor agonist phenylephrine has a positive inotropic effect but its mechanism is largely unknown. We studied the effects of phenylephrine in trabeculae isolated from three nonfailing human hearts. We found that the force of contraction rose concentration-dependently (1-300 mumol/L), maximally, to about 235% of control (at 100 mumol/L). The inositol phosphates were increased to 195-262%, whereas the phosphatidylinositol phosphate and phosphatidylinositol bisphosphate decreased to 69-73% of control. The present results suggest that the alpha 1-adrenoceptor-mediated increase in inositol trisphosphate and the positive inotropic effect may be causally related in the normal human heart.

Adult↗

Exchangeable body sodium in normal man: analysis of various frames of reference.

Exchangeable sodium is a reliable measure of body sodium contents. Since fat tissue contains significantly less sodium per unit of weight than other tissues, leanness of an individual may considerably affect exchangeable body sodium. Thus, subjects of different body size can be compared only when body build is considered. To evaluate various frames of reference, we analysed the relationship between exchangeable sodium as determined by isotope dilution and various parameters of body size. Body weight, body height, body surface area, and leanness index correlated significantly with exchangeable sodium, the closest relationship having been obtained with body surface area (r = 0.790; p less than 0.001). When analysing males and females separately (n = 18 and 36, resp.), best parallelism of regression lines was also obtained with body surface area. It is concluded that exchangeable sodium should be referred to unit of body surface area, expressing each individual's value as percent of the normal predicted value calculated from the regression equations y = 1388x + 370 and y = 1554x - 196 for males and females, respectively.

Adult↗

Triton X-100 promotes the accumulation of phosphatidic acid and inhibits the synthesis of phosphatidylcholine in human decidua and chorion frondosum tissues in vitro.

Triton X-100 is known to affect phospholipid metabolism and the generation of various signal molecules from cellular phospholipids. In the present work the effect of Triton X-100 on phospholipid metabolism of human decidua and of the primordial placenta (chorion frondosum) was studied. Triton X-100 (0.05%, v/v) added to tissue mince 30 min before the end of a 60 min incubation stimulated 2-4-fold (decidua) and 4-6-fold (placenta) the incorporation of [32P]phosphate ([32P]Pi) into phosphatidic acid, while markedly decreasing the labeling of phosphatidylcholine. Triton X-100 had no effect on the labeling of phosphatidylinositol in the decidua, and only a slight increase was observed in the placenta. When labeled glucose was used to assess phospholipid synthesis, the addition of Triton had no effect on phosphatidic acid, while decreasing the synthesis of phosphatidylcholine. Incorporation of [32P]Pi into phosphatidic acid was not accelerated by a submicellar concentration (0.01%) of Triton, whereas the synthesis of phosphatidylcholine was decreased irrespective of detergent concentration. Anionic or cationic detergents could not mimic the action of Triton on phosphatidic acid synthesis. Although Triton inhibited the synthesis of ATP in a dose-dependent manner, this could not account for the above results. Instead, it is suggested that diacylglycerol kinase and phosphocholine:CTP cytidylyltransferase are possible targets of the action of Triton X-100.

Chorion↗

Differential effect of progesterone on the labeling of phosphatidylinositol with [3H]inositol and [32P]phosphate in the uterus of the estrogen-treated ovariectomized rat.

In rat uterine mince incubated in vitro [3H]inositol was found to be incorporated into phosphatidylinositol (PI) predominantly via a pathway which could be markedly and dose dependently activated with Mn2+ (0.1-10 mM) and inhibited by Ca2+ (1-10 mM). These ions had no effect on the incorporation of [32P]phosphate (32P) into PI indicating a distinct inositol-exchange mechanism for the labeling of PI with [3H]inositol. Treatment of ovariectomized rats for 5 days with 2 micrograms estradiol dipropionate (EDP) increased about 3-fold (when measured in the presence of 1 mM Mn2+) and 4-5-fold (when measured in the presence of 1 mM Ca2+) the inositol-exchange activity in the rat uterus, and these effects were suppressed by 40 and 30% respectively by the concomitant administration of 2 mg progesterone (P). EDP alone or in combination with P increased to the same extent (by a factor of 2-3) the rate of labeling with 32P of phosphatidylcholine (PC), phosphatidylethanolamine (PE) and plasmenylethanolamine (PmE). The labeling rate of PI was increased 1.5-1.7-fold by treatment with EDP and this increase was selectively augmented further to about 2.5-fold by the simultaneous administration of P. Treatment with P alone had no significant effect on the incorporation of either labeled precursor. Steroid hormone treatments had no effect on the amount of these phospholipids in 100 mg uterine tissue, but they increased about 1.7-fold the rate of labeling of ATP with 32P. We conclude that P, when administered together with estradiol, regulates differentially the turnover of the inositol and phosphate moieties of PI with possible physiological consequences.

Adenosine Triphosphate↗

Influence of dopamine on atrial natriuretic peptide level in premature infants.

The role of dopamine (DA) in the activation and/or release of atrial natriuretic peptide (ANP) was investigated in 11 premature infants during the early postnatal period. Mean plasma concentration of ANP and free DA level before DA infusion was 252.6 +/- 210 fmol/ml, and 0.4 +/- 0.2 ng/ml, respectively. DA infusion in a dose of 2 micrograms/kg/min caused a rise in plasma free DA level to 59.7 +/- 21.5 ng/ml and a significant increase in GFR, diuresis, sodium excretion and fractional sodium excretion. The plasma concentration of ANP, however, remained unchanged (252.6 +/- 210.0 vs. 213 +/- 143.0 fmol/ml). Thus, our data failed to demonstrate a stimulatory effect of DA on ANP release in premature infants. The role of the high plasma concentration of ANP in preterm neonates immediately after birth has to be clarified.

Atrial Natriuretic Factor↗