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Biomedical subjects

E Simon

Publications and source records attributed to E Simon.

At least 181 records · Page 10Linked to original sources
PubMed1984

The effect of acetylsalicylic acid on renal function in the Pekin duck.

The acute effects of intravenously administered lysine-acetylsalicylic acid (ASA) on renal function in the Pekin duck have been studied with special reference to possible interactions with the antidiuretic hormone, arginine vasotocin (AVT), in the control of renal water and solute output. ASA produces an immediate increase in urine flow rate which is dose-related in the range 25 to 100 mg kg-1 and is associated with a slight reduction in urine osmolality, but an overall increase in renal osmolal excretion affecting Na+, Cl- and K+ to approximately equal extents. The effects, which are similar in both saltwater and freshwater adapted ducks infused with hyposmotic saline or glucose solution, can also be produced by similar doses of sodium salicylate (SA). The mechanism of action is probably not related to inhibition of prostaglandin synthetases. There is no change in the glomerular filtration rate or peripheral blood pressure following the ASA injection. There is no change in the circulating level of AVT; however, preliminary studies do not exclude the possibility of a partial antagonism of salicylate to AVT at the renal level.

Animals↗
PubMed1984

Circulatory and osmoregulatory effects of angiotensin II perfusion of the third ventricle in a bird with salt glands.

In Pekin ducks adapted to salt water, 1Asp - 5Val -angiotensin II, 1Asp - 5Ile -angiotensin II and 1Asp - 5Ile -tetradecapeptide were applied intracerebroventricularly (I.C.V.) during steady-state conditions evoked by continuous intravenous loading with 200 mosmol kg-1 saline. Each of the angiotensin II (AII) analogues caused a dose-dependent antidiuresis with a concomitant rise in urine osmolality and electrolyte concentration. Antidiuresis was linearly correlated with plasma arginine vasotocin (AVT). The elevation of plasma AVT occurred rapidly during I.C.V. stimulation with AII and declined exponentially to the pre-stimulation level. Under conditions of salt loading with 1000 mosmol kg-1 saline in which the ducks excreted the salt and water by their supraorbital salt glands, AII applied I.C.V. in a concentration of 1 nmol ml-1, inhibited the NaCl excretion via the salt glands. Arterial blood pressure and heart rate increased after I.C.V. microperfusion with 1 nmol ml-1 AII. This was not due to leakage of I.C.V. AII into the circulation because systemic application of AII required a 100-fold higher dose to elicit similar effects. Respiration rate remained constant. Systemically applied AVT which produced plasma levels similar to, or greater than, those caused by centrally acting AII resulted in the same antidiuretic responses but did not mimic the circulatory effects of I.C.V. AII. Specific AVT antiserum, injected intravenously, totally suppressed the renal response to I.C.V. AII and reduced the rise in blood pressure and heart rate by more than 50%. The anterior part of the third ventricle was more sensitive than the posterior part in eliciting the antidiuretic responses to I.C.V. applied AII. The particular combination of effects on renal excretion, salt gland secretion and cardiovascular function of centrally applied AII in the duck supports the idea that AII plays a major role as a central modulator of volume homeostasis.

Angiotensin II↗
PubMed1984

Salt gland and kidney responses to intracerebral osmotic stimulation in salt- and water-loaded ducks.

Saltwater-adapted ducks with functioning supraorbital salt glands were chronically implanted with a device for perfusion of the third cerebral ventricle (icv perfusion) with artificial cerebrospinal fluid (CSF) of different tonicities. The osmoregulatory responses to icv stimulation were studied at conditions of salt and water loading in which only the salt glands, both salt glands and urinary fluid excretion, or only urinary fluid excretion were stimulated; in the latter experiments plasma antidiuretic hormone (ADH) was measured with a radioimmunoassay. Hypertonic icv stimulation enhanced salt gland secretion and caused antidiuresis, due to the increase of plasma ADH. Hypotonic icv stimulation inhibited salt gland activity and caused diuresis, due to the decrease of plasma ADH. Salt gland activity, urine formation, and plasma ADH reacted more sensitively to changes of icv tonicity in the hypertonic than in the hypotonic range. The effect of icv hypotonic stimulation could be obtained also with icv perfusion of isosmotic artificial CSF deficient in NaCl content. Perfusion with artificial CSF exceeding plasma tonicity by 50 mosmol X kg-1 or more caused inhibition of salt gland secretion associated with enhanced urinary output in several experiments.

Afferent Pathways↗
PubMed1984

[Primary tumors of the nervous system in the light of an epidemiologic analysis].

On a territory of 5 districts of western Poland with 3.097 thousands of inhabitants the annual incidence rates per 100 thousands of population as well as the prevalence rates of primary neoplasms have been determined. The results of our investigation have shown that multiforme glioblastomas and astrocytomas occurred in the investigated population with the highest annual incidence rates, whereas the highest prevalence rates were found for hypophyseal adenomas, to be followed by astrocytomas, meningiomas and glioblastoma multiforme. The obtained results are critically discussed and compared with epidemiological data presented by other authors who based on records from neurosurgical departments and autoptic sections, it is concluded that the presented results do reflect objectively the epidemiological situation of Poland.

Adenoma↗
PubMed1984

Control of central release of vasopressin.

A diffuse extrahypophyseal vasopressinergic system has been described in the brain, and vasopressin (AVP) has also been identified in the cerebrospinal fluid (CSF) of several species. Administration of AVP to the central nervous system has been found to influence several brain functions. It has been suggested therefore that this peptide may act as a physiologically significant neuromodulator of the central nervous system functions, including the control of the body fluid homeostasis. However, the mechanisms controlling the central release of AVP are poorly recognized. The purpose of the present investigation was to find out whether the release of AVP into the CSF is controlled by volume and osmotic stimuli and whether it may be relevant to the control of water intake. The experiments were performed on conscious dogs chronically implanted with a device enabling the withdrawal of CSF from the anterior part of the third ventricle which is situated in the vicinity of abundant vasopressinergic fibers. AVP measured by radio-immunoassay and osmolality were determined in blood and CSF samples taken simultaneously. 24 h dehydration caused a significant elevation of plasma (Posm) and CSF (CSFosm) osmolalities as well as of plasma (PAVP) and of CSF (CSFAVP) AVP concentrations. During rehydration total water intake (TWI) X kg-1 b.w. was significantly correlated with Posm and PAVP as well as with CSFosm and CSFAVP prior to drinking. Rehydration caused Posm, PAVP, CSFosm and CSFAVP to decrease significantly within 90 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMed1984

Volume regulatory action of central angiotensin II in the duck.

In the Pekin duck intracerebroventricularly perfused analogues of angiotensin II stimulate the release of neurohypophyseal antidiuretic hormone (AVT) which then acts on the kidneys to reduce glomerular filtration and to increase tubular water permeability. In addition, the centrally mediated inhibition of salt and water excretion via the supraorbital salt glands, as well as vasoconstriction and tachycardia, indicate that angiotensin II plays a major role as a central modulator in the homeostasis of the volume of the extracellular fluid compartment as well as its tonicity.

Angiotensin II↗
PubMed1983

Interaction between hypothalamic and extrahypothalamic body temperatures in the control of panting in rabbits.

In conscious rabbits with chronically implanted hypothalamic thermodes sustained panting was induced by exposure to 39 degrees C ambient temperature. Core temperature (Tc) measured in the esophagus was maintained at hyperthermic levels of about 41.1, 40.2 and 39.2 degrees C by controlled heat extraction with a cooling thermode inserted into the colon. Hypothalamic temperature (Thy) was varied from its control value of 39.1 degrees C for periods of 2-3 min by altering the temperature of the water perfusing the thermode in a stepwise fashion from 39 degrees C to mostly lower and sometimes higher values. In several experiments a period of moderate hypothalamic cooling was immediately followed by a period of strong cooling. Breathing frequency (BF) was continuously recorded as an index for thermal panting. Panting rate was positively correlated with Tc, maximum panting being attained at 41.1 degrees C Tc and normal Thy. Lowering Thy reduced and elevating Thy stimulated panting at constant Tc. At each level of Tc the inhibitory effect of lowering Thy on BF was found to be diminished at strong degrees of hypothalamic cooling resulting in non-rectilinear relationships between BF and Thy. In the experiments with two-step hypothalamic cooling BF tended to rise in some trials rather than to decrease further with the transition from moderate to strong hypothalamic cooling. The relationships between Tc, Thy and BF could be satisfactorily described by each of two mathematical models, the one presuming a Q10 of 1.5 for cold and a Q10 of 8.3 for warm signal transmission in the hypothalamus, the other presuming a Q10 of 3.5 for cold and a Q10 of 2.5 for warm signal transmission and, additionally, the existence of hypothalamic thermosensors.

Animals↗
PubMed1983

A temperature-sensitive mutant of Newcastle disease virus which is affected in both haemagglutinin-neuraminidase and matrix proteins.

Virions prepared from a non-revertible temperature-sensitive (ts) mutant (ts53) of Newcastle disease virus (NDV) grown in ovo at the permissive temperature (34 degrees C) possessed thermolabile haemagglutination and neuraminidase activities compared with parental (ts+) virions. Purified haemagglutinin-neuraminidase (HN) protein from ts53 virions was also more thermolabile than ts+ HN protein. SDS-PAGE analysis of [3H]leucine pulse- and pulse/chase-labelled NDV proteins synthesized in chick embryo fibroblasts following infection with ts+ and ts53 virus revealed that ts53 matrix (M) protein was unstable and disappeared during chase incubations only at the non-permissive temperature (42 degrees C). The non-revertibility of the ts53 mutant may indicate that it is a double mutant affected in both HN and M genes; alternatively this mutant may only be affected in the HN gene, the close physical association of the thermolabile HN with the M protein during virus maturation resulting in the lack of protection of the M protein from the action of cellular proteases at the non-permissive temperature.

Cycloheximide↗
PubMed1983

Vasopressin in blood and third ventricle CSF of dogs in chronic experiments.

A device for chronic implantation was developed that allowed sampling of cerebrospinal fluid (CSF) from the anterior part of the third cerebral ventricle (A3V) of dogs in repeated experiments for up to 4 mo. Osmolalities, electrolyte concentrations, and concentrations of arginine vasopressin (AVP) measured with a radioimmunoassay were determined in repeated experiments on the chronically prepared animals under conditions of normal hydration, both in the conscious state and during inhalation anesthesia. In conscious dogs, AVP concentrations in plasma and CSF were 3.3 +/- 0.4 and 21.8 +/- 2.5 pg X ml-1, respectively. During anesthesia without surgical interference, the AVP concentrations in plasma and CSF were increased twofold above the levels obtained in conscious dogs. During the time of observation (180 min) all measured parameters remained constant. The AVP concentrations in plasma and CSF samples collected during the surgical procedure of device implantation were about 10-fold higher than in the samples collected during the conscious state. Thus, in each experimental condition, AVP concentration in the CSF collected from the A3V was consistently higher than that in the simultaneously collected blood samples.

Animals↗
PubMed1983

Handling of ammonium by the renal proximal tubule during acute metabolic acidosis.

The present studies were designed to assess the handling of ammonium (NH+4) by the proximal tubule during acute metabolic acidosis (AMA). After tubule fluid collections were obtained with micropuncture techniques and in situ pH was determined near the end of the proximal tubule, 0.2 N HCl was infused intravenously at 17 microliter X min-1 X 100 g body wt-1. Thirty to sixty minutes later, samples were obtained and pH measurements were made near the previous micropuncture sites. During AMA, urine pH fell and total acid excretion doubled due to an increase in NH+4 excretion from 581 +/- 63 to 1,153 +/- 61 nmol X min-1 X g kidney wt-1 (P less than 0.001). Acid excretion did not change in time controls. Tubule fluid NH+4 rose from 2.17 +/- 0.15 to 3.45 +/- 0.24 mM during acid infusion (P less than 0.001) and its delivery to the end of the proximal tubule nearly doubled (67.8 +/- 6.3 vs. 33.9 +/- 2.9 pmol X min X g kidney wt-1 before acid infusion, P less than 0.001). This increase in delivery during AMA was due to enhanced ammonia (NH3) entry into the proximal tubule. In situ pH determined near the end of the proximal tubule averaged 6.94 +/- 0.04 before acid infusion and did not change afterwards (6.87 +/- 0.05). These data are consistent with the hypothesis that in AMA the increase in NH+4 excretion is due primarily to an increase in the cortical production of NH3.

Acidosis, Renal Tubular↗
PubMed1983

Comparison of the interactions of soya bean protease inhibitors with rat pancreatic enzymes and human trypsin.

The present work describes the effect of two soya bean protease inhibitors: Kunitz type (SBTI) and Bowman-Birk type (BBTI) on rat trypsin I (TrI), trypsin II (TrII) and chymotrypsin (Chtr) and on human cationic trypsin (hTr). The inhibition spectra show that: (1) SBTI inhibits TrI, TrII, Chtr and hTr esterase activities by 80, 80, 83 and 45%, respectively, at inhibitor-to-enzyme molar ratios of one-to-one, and (2) BBTI inhibits TrI, TrII, Chtr, and hTr esterase activities by 50, 65, 75 and 30%, respectively, at an inhibitor-to-enzyme molar ratio of two-to-one. A similar inhibition pattern was obtained by testing proteolytic activities. It would appear that hTr is less sensitive to soya bean protease inhibitors than each of the rat proteases investigated. This difference in inhibition should be considered when a rat is used as a model to predict the effects of dietary soya bean protease inhibitors on humans.

Animals↗
PubMed1983

Effect of reduced renal mass on ammonium handling and net acid formation by the superficial and juxtamedullary nephron of the rat. Evidence for impaired reentrapment rather than decreased production of ammonium in the acidosis of uremia.

Papillary and surface micropuncture were used to study the handling of ammonium and the formation of net acid by surface nephrons, deep nephrons, and the terminal segment of collecting duct (CD) after renal mass was reduced by two-thirds. Net acid excretion by the remnant kidney (RK) was significantly reduced, averaging 794+/-81 neq/min (SE) compared with 1,220+/-105 neq/min after sham operation (P < 0.001), due to a decrease in ammonium excretion (494+/-54 vs. 871+/-79 nmol/min in controls, P < 0.001). Urinary pH and titratable acid excretion were not different in the two groups of animals. After RK formation, ammonium delivery to the end of the proximal tubule increased nearly threefold and averaged 66.2+/-5.6 compared with 18.4+/-2.9 pmol/min in controls, (P < 0.001). This greater delivery of ammonium was primarily due to renal tubule entry rather than to changes in the filtered load and was only partially related to the differences in flow rate. Ammonium processing by deep nephrons was profoundly affected by a reduction in renal mass. Although absolute delivery of ammonium was greater to the bend of Henle's loop (BHL), the difference could be accounted for on the basis of an increase in nephron size. Thus, fractional delivery (FD(NH+4)) to this site was not different for the two groups of animals, averaging 1,567+/-180% in controls and 1,400+/-181% in the group with the RK. Hydrogen secretion in the proximal segments of deep and surface nephrons did not increase in proportion to the decrease in renal mass and as a consequence bicarbonate delivery to the end of the proximal tubule of surface nephrons and to the BHL of deep nephrons was increased. When renal mass was reduced FD(NH+4) to the base of the terminal CD doubled but did not change by the tip. In both groups FD(NH+4) to the base of the CD was greater than to the end of the distal tubule. However, the increase was the same. On the other hand, the increase in the net acid index between the end of the distal tubule and the base of the CD was profoundly greater in rats with an RK. This difference was primarily due to bicarbonate reabsorption rather than enhanced ammonium reentry. Indeed, >400% of the fractional ammonium delivered to the end of the proximal tubule was lost from the tubule fluid. The data suggest that the decrease in acid excretion by the RK is due to two factors. First, hydrogen secretion in the proximal segments of both nephron populations fails to increase in the proportion to the reduction in renal mass. Second, a reduced reentrapment of ammonia, rather than its impaired production, causes ammonium excretion to decrease.

Acidosis↗