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Biomedical subjects

E Simon

Publications and source records attributed to E Simon.

At least 19 recordsLinked to original sources
PubMed1992

Effect of angiotensin II and atrial natriuretic factor on neurons in the subfornical organ of ducks and rats in vitro.

Atrial natriuretic factor (ANF) antagonizes many angiotensin II (ANGII)-induced effects on osmoregulatory relevant parameters in vivo. In this study ANF analogues decreased the spontaneous and the ANGII-induced electrical activity of subfornical organ (SFO) neurons in rats, but had no effect on ANGII sensitive or insensitive SFO neurons in ducks. These results suggest a more distinct functional separation for the responsiveness to ANGII and ANF in birds compared to mammals.

Action Potentials↗
PubMed1992

Ionic responsiveness in third ventricular hypertonic stimulation of antidiuresis in ducks.

Domestic ducks were chronically equipped with a device probing the third cerebral ventricle (VIII) for localized intracerebroventricular (i.c.v.) perfusion. In conscious animals made diuretic by intravenous water loading with 1.0 ml/min hypoosmotic glucose solution (200 mOsm/kg), hyperosmotic i.c.v. stimulations were tested for antidiuretic actions. Artificial cerebrospinal fluid made hypertonic (400 mOsm/kg) by adding sucrose, mannitol, NaCl, LiCl, choline chloride, NaI, NaNO3, LiNO3, CaCl2 or MgCl2 was perfused i.c.v. for 10-15 min at rates of 10-15 microliters/min. Arterial pressure and heart rate were monitored continuously. Hyperosmotic stimulations with non-electrolytes did not induce antidiuresis. Approximately equivalent degrees of antidiuresis were elicited by Na(+)-, Li(+)- and choline salts with a tendency for moderate rises in arterial pressure. Compared to Cl(-)- and I(-)-salts, the effects of NO3(-)-salts were attenuated. Divalent cations caused prolonged antidiuresis, sometimes preceded by initial diuresis, with circulatory side effects unrelated to the changes in renal fluid excretion. It is concluded that the observed antidiuretic effects were mediated by cation-sensitive, rather than osmosensitive neurons on the brain side of the blood-brain-barrier. Their transduction mechanism might consist of poorly selective membrane channels permeable to cations but not to anions.

Animals↗
PubMed1992

Dissociable antiviral activities directed against cardioviruses are expressed in L cells treated with interferon.

Interferon (IFN) restricts a wide variety of viruses. To do so it elicits many antiviral pathways. For example, subclones of the same cell line with a reduced antiviral spectrum are thought to lack one or more antiviral pathways. Our line of L cells exhibits two distinct antiviral activities. The first delays the yield of both wild-type mengovirus (is+) and an IFN-sensitive mutant (is-1). The second specifically inhibits is-1 virus yields 100-fold. From these cells, a subclone was isolated which had lost the second antiviral activity (i.e. in these cells is-1 virus acts like is+ virus). To see whether other cardioviruses are sensitive to these activities, two additional strains [m-mengovirus and encephalomyocarditis-R (EMC-R) virus] were tested in our subclones. Like is+ virus, m-mengovirus yields were delayed by IFN in both subclones; EMC-R virus behaved like is-1 virus in both cell lines. When actinomycin D was added at the time of infection, is-1 virus was phenotypically reversed to is+ virus, but EMC-R virus was still inhibited. The 2-5A synthetase/RNase L pathway is expressed in both clones. Therefore, at least three antiviral activities against cardioviruses can be distinguished in IFN-treated L cells, and two of them appear not to involve the 2-5A synthetase/RNase L pathway.

Animals↗
PubMed1992

Inhibition of vasopressin and aldosterone release by atrial natriuretic peptide in conscious rabbits.

To elucidate the regulatory role of atrial natriuretic factor (ANF) on vasopressin (AVP) and aldosterone release in conscious rabbits, ANF was administered systematically at a rate of 15 pmol min-1 (kg body wt)-1 for 15 min in two series of experimental animals in which AVP and/or aldosterone production was stimulated. In euhydrated rabbits (series I), systemic administration of angiotensin II (Ang II) (10 pmol min-1 (kg body wt)-1, 15 min) stimulated aldosterone release threefold from basal plasma concentrations (140 pg ml-1). The co-application of ANF inhibited the Ang II-induced release of aldosterone without influencing the non-stimulated AVP system. In dehydrated rabbits (series II) with elevated plasma osmolality and AVP concentration, exogenously applied ANF increased plasma ANF fourfold at marginally reduced arterial pressure. Plasma AVP concentrations were reduced by 3.4 pg ml-1 (25%) on average, and plasma aldosterone concentrations were lowered by 34 pg ml-1 (23%) at unchanged levels of plasma corticosterone. Receptor binding studies using [125I]ANF as radioligand revealed Ang II-independent high-affinity receptors for ANF in the zona glomerulosa of the adrenal gland. With regard to the hypothalamo-neurohypophyseal AVP system, ANF binding sites were localized to the median eminence and neurohypophysis, but not to the magnocellular nuclei. ANF receptors were also labelled in structures lacking a blood-brain barrier such as the subfornical organ and the choroid plexus.

Adrenal Glands↗
PubMed1992

Central ANP administration in conscious dogs responding to dehydration and hypovolemia.

Eighteen beagles were chronically instrumented with an anterior third ventricular (A3V) infusion device to analyze, in conscious dogs, the involvement of central atrial natriuretic peptide (ANP) in body fluid and blood pressure control. The dogs' osmotic and body fluid homeostasis was challenged by 24 h water deprivation or blood withdrawal (12 ml/kg body wt) to elucidate possible modifying influences on the release of arginine vasopressin (AVP), angiotensin II (ANG II), and drinking. Three series of experiments were performed: 1) infusion of ANP (500 ng/min) dissolved in artificial cerebrospinal fluid (aCSF) and given for 10 min, 2) infusion of aCSF alone for the same length of time, and 3) time control experiments without infusion. Plasma AVP and ANG II were analyzed by radioimmunoassay, and in several experiments on dehydrated dogs, plasma norepinephrine and epinephrine were additionally determined by high-performance liquid chromatography. Various blood parameters and rectal and ear skin temperatures were measured. Arterial pressure and heart rate were recorded in three animals additionally equipped with carotid loops. Changes in plasma AVP and ANG II induced by dehydration and bleeding were not significantly modified by A3V infusions of ANP and aCSF in comparison to time controls. Blood pressure changes were similar in experiments with A3V ANP infusion and time controls during bleeding and reinfusion. It is concluded that central ANP is not important in the control of vasopressin and renin-angiotensin systems during osmotic and volume challenges in conscious dogs.

Animals↗
PubMed1992

Alteration of endotoxin fever and release of arginine vasopressin by dehydration in the guinea pig.

Arginine vasopressin (AVP), synthesized in hypothalamic neurons, is transported in axons either to the pituitary for release into the circulation or to different brain areas. In our previous experiments we documented central antipyretic AVP pathways from the hypothalamus to the ventrolateral septal area in the limbic system. In the present study we investigated if osmotic stimulation is able to activate peripheral and central release of AVP concurrently and if the antipyretic pathways are influenced by this kind of stimulation. In dehydrated animals (24 h water deprivation) the arterial blood plasma level of AVP doubled causing antidiuretic effects. Also the concentration of AVP in push-pull perfusates of the limbic septal area was significantly higher in dehydrated (5.6 pg AVP/ml perfusate) than in control animals (2.6 pg AVP/ml perfusate). The febrile response to bacterial endotoxin was reduced by 50% in dehydrated guinea pigs compared to controls, statistically significant between 30 and 180 min after pyrogen application. A microinfusion of AVP antiserum into the limbic septal area enhanced the fever reaction of dehydrated guinea pigs compared to the effects of a microinfused preimmune serum, in this case statistically significant between 180 and 360 min after application. From these data we assume a simultaneous activation of peripheral and central release of AVP with antidiuretic and antipyretic effects by dehydration.

Animals↗
PubMed1992

[Medical interruption of pregnancy. Indications and techniques. Critical study and reflections on 324 cases].

A retrospective study of 324 cases highlights the difficulties encountered in identifying indications for medical pregnancy terminations (MPTs) which are permitted by French law and medically justified. In addition, the ethical problems raised do not facilitate the decision to opt for a MPT, which must be made by a multi-disciplinary committee. The methods used to evaluate the pregnancy are largely surgical during the first three months, and these are succeeded during the next six months by medical methods involving the use of synthetic prostaglandins. The complications which may occur are far from minor. The various protocols used by the authors are described together with their results and complications.

Abortion, Therapeutic↗
PubMed1991

[Congestive gastropathy].

15 patients with congestive gastropathy were reported including clinical and pathological characteristics of the disease. Every patient had alcoholic liver cirrhosis and portal hypertension. 6 patient's stomach was resected while in 2 further cases the disease was found at autopsy. In additional 7 cases the characteristic microvascular changes were observed in endoscopic biopsy specimens from the gastric mucosa. The authors presume that this disease has an acute and a chronic stage. In the acute stage dilated capillaries are present under the surface, not related to the inflammation of gastric mucosa. This phenomenon was described in the literature. In the chronic stage there are dilated and tortuous vessels in the submucosal layer surrounded by collagenous connective tissue. The authors suppose that the thick and fibrotic submucosal layer causes microcirculatory disturbances in the gastric mucosa. The impaired microcirculation may cause extensive ulcers with profuse and sometimes lethal bleeding.

Adult↗
PubMed1991

Analysis of children's word-finding skills in discourse.

This investigation analyzed children's word-finding skills in discourse. The subjects, 16 children with word-finding problems and 16 normal children in Grades 1-6, were matched for sex, age, grade, ethnicity, socioeconomic status, geographic region, and receptive language. Subjects' narratives, produced in response to three pictures and five probes, were tape recorded, transcribed, and analyzed with respect to the following word-finding indices: language productivity and the incidence of word-finding characteristics (repetitions, reformulations, substitutions, delays, empty words, time fillers, and insertions). Group comparisons were made with respect to these indices. Children with word-finding disorders did not differ from normal children in language productivity but manifested significantly more word-finding characteristics in their narratives. These findings are discussed with respect to characteristics and assessment of and intervention for children with word-finding disorders in discourse.

Child↗
PubMed1991

Control of renal handling of potassium loads in ducks with active salt glands.

Domestic ducks adapted to saline of 400 mosmol/kgH2O as their only water supply received intravenous loads of 100 mM KCl for 2 h while being intravenously infused with 200 mM NaCl at 1.0 ml/min to produce simultaneous salt gland secretion and diuresis-natriuresis. K+ loading did not alter the plasma levels of the osmoregulatory hormones arginine vasotocin, angiotensin II, aldosterone, and atrial natriuretic factor but promptly evoked kaliuresis because of a rise from 17 to 155 mM in urinary K+, with a proportional decrease in urinary Na+. Continuous infusion of amiloride (0.04 mg.min.-1.kg body wt-1 iv) further enhanced diuresis and natriuresis and lowered urinary K+, but the kaliuretic response to K+ loading was only moderately reduced because of enhanced diuresis and a rise in urinary K+ from 3 to 33 mM, with a slight decrease in urinary Na+. Changes in plasma hormone levels reflected dehydration due to excessive diuresis but were not related to kaliuresis. Salt gland secretion was not affected directly by amiloride but was secondarily reduced by the induced dehydration. In amiloride-treated ducks, hyperkalemia in response to K+ loading was exaggerated relative to the modest reduction in K+ excretion and may be attributed to moderate metabolic acidosis and/or general effects of amiloride on K+ metabolism. It is concluded that none of the established osmoregulatory hormones is involved in short-term control of renal K+ handling in ducks and that distal tubular K+ excretion involving amiloride-sensitive Na+ channels is quantitatively unimportant in this avian species.

Amiloride↗
PubMed1991

Transforming mechanism of the feline sarcoma virus encoded v-fms oncogene product.

The v-fms oncogene product encoded by the McDonough strain of feline sarcoma virus (SM-FeSV) is a transmembrane glycoprotein which belongs to the tyrosine kinase receptor family. The cellular counterpart, the c-fms product, is the receptor for macrophage colony stimulating factor (M-CSF or CSF-1). The v-fms and the c-fms product differ structurally only in seven point mutations and in their C-terminal domains. We have corrected the published sequence of the v-fms product and found that the new C-terminal end contains a threonine phosphorylation site (Thr939). This site is phosphorylated in vivo leading to an enhancement of the v-fms-specific tyrosine kinase activity. The extracellular domain of the v-fms product contains 11 N-glycosylation sites. Glycosylation and transport of the v-fms molecules to the plasma membrane are prerequisites for the transforming potential of the virus. Phosphorylation of the v-fms molecules in tyrosine, serine and threonine residues takes place only at the plasma membrane. Coexpression showed that the overexpression of M-CSF and c-fms in fibroblasts leads to cell transformation by an autocrine loop mechanism. This interaction between M-CSF and the c-fms protein also takes place at the plasma membrane. To study the v-fms transforming mechanisms, we have expressed the v-fms oncogene in chicken fibroblasts which are free of the cross-reactive M-CSF. The expression of the v-fms oncogene alone did not cause transformation. However, upon addition of M-CSF, these cells became completely transformed.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMed1990

Arterial hypotension in ducks adapted to high salt intake.

A homogeneous group of 8-week-old Pekin ducks was divided into two groups: saltwater (SW) ducks received salt water of gradually increasing salinity (200-600 mOsm.kg-1) from the 8th to 20th week of age; freshwater (FW) ducks were maintained on fresh water but otherwise treated identically. During the course of salt-adaptation SW ducks increased plasma osmolality, Na+ and Cl- levels, and concentrations of the osmoregulatory peptide hormones arginine vasotocin and angiotensin II. The apparent volume of inulin distribution decreased in SW ducks, but blood volume was not reduced. SW ducks also developed arterial hypotension, bradycardia, and reduced cardiac output in the course of salt adaptation. This depressed cardiovascular performance was associated with enhanced vagal restraint of cardiac function and reduced plasma concentrations of norepinephrine. Salt water adaptation did not alter the degrees to which mean arterial pressure and heart rate changed in response to intravenous bolus injections of catecholamines. The same applied to the osmoregulatory peptides which were, however, effective only at supraphysiological concentrations. The Pekin duck, as a bird predisposed for adaptation to high salt loads, presumably adapts to chronic hypertonic saline intake by resetting the central autonomic control of blood pressure to a lower level.

Adaptation, Physiological↗
PubMed1990

Platelet function after intramuscular diclofenac.

A randomised double-blind controlled study was performed to examine the effect of diclofenac on skin bleeding time and in vitro whole blood platelet aggregation. Twenty thoracotomy patients were studied; 10 were given diclofenac 75 mg intramuscularly at induction of anaesthesia, and 10 formed a control group. Skin bleeding times and platelet aggregation tests were performed the day before and repeated one hour after induction of anaesthesia. Diclofenac prolonged skin bleeding time and reduced platelet aggregation. There were no significant changes in the control group.

Adult↗
PubMed1990

Locations and properties of angiotensin II-responsive neurones in the circumventricular region of the duck brain.

1. In brain slice preparations from the hypothalamus of domestic ducks, single-unit activity was recorded extracellularly to investigate location and properties of angiotensin II (AngII)-responsive neurones in various periventricular regions. 2. When exposing the slice to 10(-7) M-AngII in the perfusion medium, more than 65% of the neurones recorded in the subfornical organ (SFO) were activated (49 out of 75) and none inhibited. In the magnocellular (MC) region of the paraventricular nucleus (PVN) only four out of eighty-one neurones were influenced by AngII; one was inhibited and three were activated. In the anterior third ventricle region (A3V) two out of twenty-one neurones were activated by AngII. In the dorsal periventricular (PeV) region, one out of thirty-seven neurones was activated and one inhibited. The changes in firing rate of AngII-responsive neurones at comparable doses of AngII were generally large in the SFO and A3V but were small in neurones from the MC and PeV regions. 3. Analysis of AngII-responsive SFO neurones consistently revealed a dose-dependent stimulation with a threshold at 10(-9) M-AngII. The AngII antagonist 1Sar-8Ile-AngII (4 x 10(-7) to 10(-6) M) caused reversible, complete or partial suppression of responsiveness to 10(-7) M-AngII. Synaptic blockade with a medium low in Ca2+ and high in Mg2+ did not abolish AngII responsiveness in eight out of ten SFO neurones tested. 4. Angiotensin III affected neither AngII-responsive nor AngII-insensitive neurones. When eighteen AngII-responsive neurones were exposed to hypertonic stimulation (+20 to +30 mosmol/kg) by adding NaCl to the perfusion medium, only one neurone was stimulated and two were inhibited. 5. The results indicate that: (a) the SFO is a specific target for circulating AngII; (b) although neurones in the A3V responsive to AngII are rare, the pronounced excitation of those which were found suggest that neurones in this region might serve as targets for AngII acting from the brain side; (c) neurones in the MC region do not seem to function as direct AngII targets; (d) neuronal AngII responsiveness in the duck's hypothalamus seems to be specific inasmuch as activation by AngII (i) is readily blocked by an AngII antagonist, (ii) cannot be induced by AngIII, and (iii) is not associated, as a rule, with responsiveness to hypertonic stimulation.

Action Potentials↗
PubMed1990

Increase in basal firing rate and sensitivity to angiotensin II in subfornical organ neurones of ducks adapted to salt water.

1. The influence of salt adaptation on spontaneous firing rate of subfornical organ (SFO) neurones and on their responsiveness to angiotensin II (AngII) (10(-10)-10(-7) M) were studied in vitro on hypothalamic brain slices taken alternately from ducks kept on either fresh water (FW ducks) or saline of 500 mosmol/kg for 8 weeks (SW ducks) as their only water supply. The animals were of the same age and were housed and fed identically. In SW ducks plasma osmolality and AngII plasma concentrations were typically increased. 2. Recording SFO single-unit activity in the AngII-free control perfusion medium disclosed significantly higher spontaneous firing rates in SW than in FW ducks with an average difference of 2.5 spikes/s. 3. With approximate threshold concentrations of AngII for activation of SFO neurones of 10(-10) M in slices from SW ducks and of 10(-9) M in slices from FW ducks, the fractions of neurones excited by AngII increased dose dependently in each group and were consistently larger in the slices from SW ducks. Average maximum increases in discharge rate during AngII-induced excitation also increased dose dependently and were higher at each AngII dose in SFO neurones from SW as compared to FW ducks. 4. Mean latencies of neuronal excitation decreased with increasing AngII doses in both groups of neurones but were significantly shorter in slices from SW than FW ducks. The shorter latencies in SW ducks corresponded to their enhanced sensitivity to AngII. Mean half-times of the disappearance of AngII-induced activation were determined after stimulation with 10(-7) M-AngII and were identical in SW and FW ducks, indicating no difference in kinetics in AngII-neurone interaction. 5. AngII-responsive SFO neurones in slices from SW ducks did not respond to AngIII and activation by AngII was abolished in the presence of the specific antagonist 1Sar-8Ile-AngII. 6. In the magnocellular portion of the paraventricular nucleus, the occurrence of AngII-responsive neurones was as infrequent in SW ducks (2 out of 45) as in FW ducks (0 out of 36). 7. The results indicate that adaptation to salt water in ducks selectively enhanced basal activity and responsiveness to AngII of the SFO neurones. This is a functional correlate of the up-regulation of AngII-receptor density observed in the SFO of the same species in the course of adaptation to salt water. Both adaptive adjustments seem to provide tighter coupling between systemic and central control of salt and fluid balance in conditions of chronic salt stress.

Action Potentials↗
PubMed1990

Differential osmoresponsiveness of periventricular neurons in duck hypothalamus.

Single-unit responses to osmotic stimulation were recorded extracellularly in slice preparations from the duck's hypothalamus in the periventricular layer (pl), magnocellular center (mc), and deep periventricular neuropil of the paraventricular nucleus (PVN). The pl neurons were located in the dorsorostral third ventricular region of maximum osmoresponsiveness determined in vivo. Hypertonic stimulation (+20 to +35 mosmol/kgH2O) by excess NaCl in the incubation medium excited 25 and inhibited 4 out of 48 pl neurons. Hypotonic (-10 to -20 mosmol/kgH2O) stimulation inhibited 9 out of 10 neurons activated by hypertonic stimulation. Hypertonic activation of pl neurons was maintained in seven out of nine neurons when NaCl was replaced by LiCl, but replacing NaCl by sucrose was ineffective in each of 10 neurons. Synaptic blockade (Ca2(+)-free/high-Mg2+ medium) did not abolish hypertonic activation in 8 out of 11 pl neurons. Among 30 mc neurons, 2 were activated and 1 inhibited by hypertonic stimulation with NaCl (+20 to +35 mosmol/kgH2O), and among 24 neurons in the periventricular neuropil, 2 were activated and 4 inhibited. The function of osmoresponsive pl neurons as specific receptors would be consistent with their morphological characteristics and with the location and functional properties of the duck's third ventricular osmoresponsiveness in vivo.

Animals↗