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Biomedical subjects

I Barna

Publications and source records attributed to I Barna.

15 recordsLinked to original sources
PubMed1992

Effects of mediobasal hypothalamic lesion on immunoreactive ACTH/beta-endorphin levels in cerebrospinal fluid, in discrete brain regions, in plasma, and in pituitary of the rat.

One week after complete destruction of the mediobasal hypothalamus, immunoreactive adrenocorticotropin (ACTH) and beta-endorphin levels were determined in cerebrospinal fluid, trunk blood, as well as in brain and pituitary tissue samples collected from anaesthetized and cisternally cannulated rats. Control rats were sham operated. In lesioned rats we observed: (a) 60% decrease in the immunoreactive beta-endorphin concentrations in the cerebrospinal fluid, (b) decreased immunoreactive ACTH and beta-endorphin levels in the hypothalamus, in the thalamus and in the amygdala, (c) unaffected immunoreactive ACTH/beta-endorphin levels in the septum and in the hippocampus, (d) decreased immunoreactive beta-endorphin levels both in the anterior and neurointermediate pituitary but unchanged immunoreactive ACTH contents in the anterior lobe, and (e) unaffected immunoreactive ACTH and beta-endorphin levels in the plasma under stressful conditions. From these findings the following conclusions can be drawn: (1) more than 50% of the beta-endorphin-like peptide content of the cerebrospinal fluid originates from the periventricular nuclei of the hypothalamus and thalamus in the rat; (2) the loss of the hypothalamic control probably enhances the intracellular proteolytic degradation of beta-endorphin both in the anterior and neurointermediate pituitary lobe; (3) rats with mediobasal hypothalamic lesion cannot react to the stressful stimuli of ether anaesthesia or cisternal cannulation with elevated plasma immunoreactive ACTH and beta-endorphin levels.

Adrenocorticotropic Hormone↗
PubMed1992

Immunoreactive ACTH in the cerebrospinal fluid of the rat: decrease after mediobasal hypothalamic lesion and hypophysectomy, increase after adrenalectomy.

The effect of various anaesthetics and of the manipulations of the hypothalamo-pituitary-adrenocortical system (hypophysectomy, adrenalectomy and lesion of the mediobasal hypothalamus) was studied on immunoreactive-ACTH levels in the plasma and in the cerebrospinal fluid in the rat. The anaesthetics used (Hypnorm, pentobarbital, urethan and Ketanest) were without effect on immunoreactive-ACTH concentration in the cerebrospinal fluid. Immunoreactive-ACTH was significantly decreased after hypophysectomy and elevated after adrenalectomy in both cerebrospinal fluid and plasma. Destruction of the mediobasal hypothalamus resulted in reduced immunoreactive-ACTH content in the cerebrospinal fluid (about 20% of control) in both experiments, whereas immunoreactive-ACTH levels in the plasma of the lesioned rats were lower only in one of the two experiments performed. These data suggest that the main source of the immunoreactive-ACTH in the cerebrospinal fluid of the rat is the hypothalamus; the contribution of the pituitary gland being less than 50% of the radioimmunoassayable ACTH.

Adrenalectomy↗
PubMed1992

Body sodium, atrial natriuretic peptide and blood pressure in diabetes mellitus.

Diabetes mellitus (DM) is frequently associated with hypertension for which an independent pathomechanism has been suggested. We studied 26 patients with insulin-dependent (IDDM) and 18 patients with non-insulin-dependent (NIDDM) uncomplicated DM; all patients were in metabolic balance and none of them had hypertension. Exchangeable body sodium (NaE was estimated by isotope dilution, using appr. 1.1 Mbq 24NA. In a subset of 8 IDDM and 8 NIDDM patients atrial natriuretic peptide (ANP) plasma concentration was determined prior to and after the infusion of 2000 ml physiological saline over 2 hr. NaE was significantly increased both in IDDM and NIDDM patients (104.4 +/- 11.4% and 109.9 +/- 8.0% of the normal value for healthy subjects of identical body surface area; p < 0.05 and < 0.001 resp.). Mean blood pressure (MBP) correlated significantly with NaE in both groups (r = 0.364 and r = 0.520; p < 0.05 and < 0.025, resp.) but not in healthy control subjects (r = 0.112; N.S.). Resting ANP levels were not significantly different in IDDM (34.9 +/- 11.3 pg/ml), NIDDM (42.6 +/- 11.7 pg/ml) or control subjects (40.9 +/- 17.2 pg/ml) however the infusion of saline resulted in a significantly greater increase of plasma ANP in the NIDDM patients (to 82.9 +/- 43.2 pg/ml; P < 0.01) than in the controls (55.6 +/- 23.7 pg/ml; P < 0.01) which was associated with a significantly less increase in sodium excretion (UNAV) in the NIDDM patients (+86% vs. 3170%; P < 0.02) indicating down-regulation of ANP receptors in the kidney of NIDDM patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1991

Atrial natriuretic peptide (ANP) in patients with chronic renal failure on maintenance haemodialysis.

Atrial natriuretic peptide (ANP), a recently discovered cardiac hormone, is an important regulator of body fluid homeostasis. Twenty patients with established chronic renal failure and on maintenance haemodialysis were studied before and after dialysis with capillary dialysers. ANP was determined by RIA after extraction. Mean (+/- SD) pre-dialysis ANP concentration was 146 +/- 51 pg/ml and decreased significantly during dialysis to 68 +/- 38 pg/ml (p less than 0.001). Per cent and absolute changes in plasma ANP level correlated significantly with concomitant changes in body weight (r = 0.764; p less than 0.001 and r = 0.558; p less than 0.01, resp.) but not with changes in serum creatinine, blood pressure or serum electrolytes. The obtained results indicate that ANP levels in patients with chronic renal failure are elevated mainly due to fluid overload, and the rapid fall in ANP concentration observed during haemodialysis is caused by the removal of excess fluid from the body.

Adult↗
PubMed1991

Effect of anaesthetics on the release of beta-endorphin-immunoreactivity in rat plasma.

Analgesia and anaesthesia produced by fentanyl, urethane and ether, but not pentobarbital, occurred concomitantly with an increase in the concentration of plasma beta-endorphin like immunoreactivity (BEIR), probably of pituitary origin. This increase was not associated with significant changes in pituitary or brainstem beta-endorphin content. Pretreatment with naloxone caused a reduction in plasma BEIR increase following Hypnorm, ether and urethane; and in the analgesia following Hypnorm and urethane. Pentobarbital, alone or in combination with naloxone, did not increase the concentration of plasma beta-endorphin. These results may indicate participation of endogenous opioids in the mechanism of action of urethane.

Analgesics↗
PubMed1991

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↗
PubMed1990

[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↗
PubMed1990

Disturbed hypothalamic blood flow autoregulation in the rat following hypophysectomy: a role of pituitary beta-endorphin?

The effect of hypophysectomy on hypothalamic blood flow autoregulation was studied in anesthetized, artificially ventilated rats. Local hypothalamic blood flow (HBF, H2-gas clearance method) was measured. Efficiency of autoregulation was tested by determining HBF during standardized hemorrhagic hypotension when systemic arterial pressure was lowered to 80, 60 and 40 mm Hg by consecutive, step-wise bleeding. HBF autoregulation was well maintained until 80 mmHg, but not completely at 60 and 40 mmHg arterial pressure in the sham-operated control group. In contrast, autoregulation was abolished at all levels in the hypophysectomized rats: HBF followed the changes in arterial pressure in these animals. Following hypophysectomy, the concentration of immunoreactive beta-endorphin (beta-EP) decreased drastically in plasma but remained unchanged in cerebrospinal fluid. Administration of beta-EP (200 pg/100 g b. wt.) to hypophysectomized rats by the intravenous route had no effect on autoregulation, while intracerebroventricular administration of the same dose restored autoregulation. The present findings suggest that the pituitary plays a role in hypothalamic blood flow autoregulation.

Animals↗
PubMed1990

Effects of pituitary beta-endorphin secretagogues on the concentration of beta-endorphin in rat cerebrospinal fluid: evidence for a role of vasopressin in the regulation of brain beta-endorphin release.

The concentration of beta-endorphin-immunoreactivity (beta E-IR) in cerebrospinal fluid (CSF) and plasma of rats was determined following intracerebroventricular (ICV) treatment of conscious animals with substances known to stimulate the release of beta E and other pro-opiomelanocortin (POMC)-derived peptides at the level of the anterior and intermediate lobes of the pituitary. The beta-adrenoceptor agoinst isoproterenol (ISO) did not influence the concentration of beta E-IR in CSF collected 5-60 min after ICV administration of doses ranging from 3 to 30,000 pg/rat. Plasma beta E-IR levels, however, were significantly increased 20 min following ICV injection of 30,000 pg ISO. ICV treatment of animals with ovine corticotropin-releasing factor (CRF; 30-30,000 pg/rat) also did not affect CSF levels of beta E-IR, whereas CRF in a dose of 30 pg significantly decreased, and in doses of 300-30,000 pg enhanced plasma beta E-IR concentrations as determined by 20 min following treatments. ICV injection of arginine8-vasopressin (AVP) in doses of 10-1,000 pg/rat dose-dependently elevated the beta E-IR concentration in CSF without affecting plasma beta E-IR levels. This AVP-induced increase in CSF beta E-IR was maximal 20-35 min and beta E-IR levels had returned to basal 60 min following treatment. The data indicate that AVP and not ISO and CRF is a stimulator of CSF levels of beta E-IR. As beta E-IR in CSF likely originates from brain POMC neurons, these results suggest the hot vasopressin may be a physiological regulator of brain POMC activity, and may act as a releasing factor for POMC-derived peptides in the brain.

Animals↗
PubMed1990

Vasopressin enhances the clearance of beta-endorphin immunoreactivity from rat cerebrospinal fluid.

The effect of intracerebroventricular (lateral ventricle) administration of arginine8-vasopressin (AVP) on the concentration of beta-endorphin immunoreactivity in the cerebrospinal fluid obtained from the cisterna magna was studied in rats. A decrease was observed 5 min following injection of 0.9 fmol AVP. No statistically significant changes were found 5 min after intracerebroventricular treatment of rats with 0.09 or 9 fmol. The decrease induced by 0.9 fmol AVP was of short duration and was found 5 min after treatment but not 10 and 20 min. Desglycinamide9-AVP (0.97 fmol), [pGlu4, Cyt6]-AVP-(4-9) (1.44 fmol), N alpha-acetyl-AVP (0.88 fmol), lysine8-vasopressin (0.94 fmol) and oxytocin (1 fmol) when intracerebroventricularly injected did not affect the levels of beta-endorphin immunoreactivity in the cerebrospinal fluid 5 min later. This suggests that the intact AVP-(1-9) molecule is required for this effect. Intracerebroventricular pretreatment of rats with the vasopressin V1-receptor antagonist d(CH2)5Tyr(Me)AVP (8.63 fmol) completely blocked the effect of AVP (0.9 fmol). In order to investigate further the underlying mechanism, the effect of AVP on the disappearance from the cerebrospinal fluid of exogenously applied beta-endorphin was determined. Following intracerebroventricular injection of 1.46 pmol camel beta-endorphin-(1-31), the beta-endorphin immunoreactivity levels in the cisternal cerebrospinal fluid increased rapidly, and reached peak values at 10 min. The disappearance of beta-endorphin immunoreactivity from the cerebrospinal fluid then followed a biphasic pattern with calculated half-lives of 28 and 131 min for the initial and the terminal phase, respectively. Treatment of rats with AVP (0.9 fmol; icv) during either phase (10, 30, 55 min following intracerebroventricular administration of 1.46 pmol beta-endorphin-(1-31)) significantly enhanced the disappearance of beta-endorphin immunoreactivity from the cerebrospinal fluid. The data suggest that vasopressin plays a role in the regulation of beta-endorphin levels in the cerebrospinal fluid by modulating clearance mechanisms via V1-receptors in the brain.

Animals↗
PubMed1989

Postnatal development of parthenogenetic in equilibrium with fertilized mouse aggregation chimeras.

Chimeras were made from parthenogenetic and fertilized cleavage-stage mouse embryos. The perinatal mortality was high. The parthenogenetic contributions to different tissues at birth ranged from 0 to 50%. No selection of parthenogenetic cells was observed in the pigmentation of the coat, but this does not exclude that such selection could act in other tissues. The weight of chimeras at birth negatively correlated to the average contribution of the parthenogenetic part. The growth rate of chimeras was lower than that of nonchimeric animals. The data presented demonstrated that, although parthenogenetic cells are not cell lethals and they can participate to some degree in normal development of most tissues, their extensive presence reduces the viability of chimeras and retards the postnatal development.

Animals↗
PubMed1988

Differential effects of cisterna magna cannulation on beta-endorphin levels in rat plasma and cerebrospinal fluid.

The concentration of beta-endorphin-like immunoreactivity (beta-ELIR) was determined in plasma and cerebrospinal fluid (CSF) of rats at various times following the implantation under Hypnorm anesthesia of a permanent cannula into the cisterna magna. Plasma beta-ELIR levels were highly increased immediately after the operation, and gradually returned to basal within 6 h. The beta-ELIR concentration in CSF followed a completely different pattern. It appeared to be rather stable during the first hour after the operation, was decreased at 2 h, and showed a marked increase 24 h after surgery. Two days after the surgery, beta-ELIR levels in CSF had decreased to a stable basal level which was maintained for at least 7 days. When at this stage animals were treated with Hypnorm, plasma beta-ELIR was again highly increased 30 min and not 24 h after injection, but no changes were found in the beta-ELIR concentration in CSF. These data indicate that implantation of a cannula into the cisterna magna induces postoperative changes in the CSF levels of beta-endorphin that are detectable up to at least 24 h later. Moreover, the lack of correlation between CSF and plasma levels of beta-ELIR points towards differences in the regulation of brain and pituitary pro-opiomelanocortin cells.

Animals↗
PubMed1975

The effect of enhancing factor on the immunity of mice against tetanus.

Enhancing factor was prepared from spleens of mice primed and reinjected with tetanus toxoid. The culture supernatant was separated by gel chromatography on Sephadex G-150, the resulted fractions were ultrafiltered and their enhancing activity was tested in vivo. The 1st fraction separated by gel chromatography proved to be active.

Animals↗
PubMed1975

The application of polyvalent horse immune sera for electroimmunodiffusion methods.

Horse immune sera do not give satisfactory results in immunochemical techniques based on electrophoresis of antigens through antibody-containing agarose gel. As the majority of precipitating horse antibodies belongs to the beta globulins, they migrate in the gel during electrophoresis. After enzymatic treatment the pepsin fragments work well in all electroimmunodiffusion methods.

Animals↗