Mechanism of osmosis

Osmosis is a phenomenon of paramount significance for the transport of water and solutes through biological membranes. It accounts for fluid transport out of the kidney tubules and the gastrointestinal tract, into capillaries, and across cell membranes. The thermodynamic equations for osmosis are well established [1], but, despite the fundamental significance for biological fluid transport, an understanding of osmosis at the molecular level has been lacking

Mechanism of osmotic diuresis

Mechanism of osmotic diuresis. Mannitol might inhibit para-cellular reabsorption of water and sodium chloride in the proximal tubules by reducing the osmotic driving force. We examined this hypothesis in anesthetized dogs. Bicarbonate reabsorption was kept constant by sodium bicarbonate infusion, and transcellular sodium chloride reabsorption was inhibited by ethacryn-ic acid. The glomerular filtration rate (GFR) was varied by altering renal perfusion pressure. Mannitol infusion reduced sodium chloride reabsorption from 62 ± 5% to 33 ± 5% of the filtered load. The calculated increase in reabsorbate osmolality, averaging 82 ± 6 mOsm/kg H2O, was due to sodium bicarbonate and equalled the increase in plasma osmolality. Mannitol concentration averaged 81 ± 7 mM in plasma and 101 ± 12 mM in urine. A linear relationship between reabsorption and GFR (glomerulotubular balance) was mantained over the same range of GFR before and after mannitol infusion. Mannitol infusion reduced sodium chloride reabsorption from 2.6 to 1.4 moles for each mole of sodium bicarbonate reabsorbed. During mannitol infusion, acetazolamide inhibited sodium bicarbonate reabsorption as in control experiments, but reduced sodium chloride reabsorption less. We conclude that reduced water reabsorption increases sodium bicarbonate concentration in the paracellular fluid as much as mannitol concentration is raised in the plasma and glomerular filtrate. Along the proximal tubules, net osmotic force is progressively reduced as mannitol concentration rises, accounting for reduced water and sodium chloride reabsorption.Mécanisme de la diurèse osmotique. Le mannitol peut inhiber la réabsorption paracellulaire d'eau et de NaCl dans les tubes proximaux par la réduction de la force osmotique. Pour étudier cette hypothèse la réabsorption de bicarbonate a été maintenue constante par la perfusion de bicarbonate de sodium et la réabsorption transcellulaire de chlorure de sodium a été inhibée par l'acide éthacrynique chez le chien anesthésié. Des variations du débit de filtration glomérulaire (GFR) ont été obtenues par des modifications de la pression de perfusion rénale. La perfusion de mannitol a réduit la réabsorption de chlorure de sodium de 62 ± 5% à 33 ± 5% de la charge filtrée. L'augmentation calculée de l'osmolalité de réabsorbat, en moyenne de 82 ± 6 mOsm/kg H2O, est due à bicarbonate de sodium et égale l'augmentation de l'osmolalité plasmatique. La concentration de mannitol était en moyenne de 81 ± 7 mM dans le plasma et de 101 ± 12 mM dans l'urine. Une relation linéaire entre la réabsorption et GFR (équilibre glomérulo-tubulaire) était maintenue dans le même éventail de valeurs de GFR avant et après perfusion de mannitol. La perfusion de mannitol diminue la reabsorption de chlorure de sodium de 2.6 à 1,4 moles pour chaque mole de bicarbonate de sodium réabsorbée. Pendant l'infusion de mannitol, l'acétazola-mide a inhibé la réabsorption de bicarbonate, autant que dans les contrôles, tandis que la réabsorption de chlorure de sodium a été moins réduite. Nous concluons que la diminution de réabsorption d'eau augmente la concentration de bicarbonate de sodium dans le liquide paracellulaire dans la mesure où la concentration de mannitol est augmentée dans le plasma et le filtrat glomérulaire. Le long des tubes proximaux la force osmotique nette est progressivement réduite au fur et à mesure que la concentration de mannitol augmente, ce qui rend compte de la diminution de réabsorption d'eau et de chlorure de sodium

Hypernatremia inhibits NaHCO3 reabsorption and associated NaCl reabsorption in dogs

Hypernatremia inhibits NaHCO3 reabsorption and associated NaCl reabsorption in dogs. To examine the effect of selective rise of plasma NaCl concentration (hypematremia) on NaHCO3 reabsorption and associated NaCl reabsorption remaining during continuous ethacrynic acid infusion, hypertonic NaCl solution was infused in three groups of anesthetized volume-expanded dogs. In six dogs examined at constant hematocrit and plasma pH, bicarbonate and water reabsorptions were inversely related to PNa and reduced by 37% and 39% respectively by raising PNa from 140 to 200 mM. Chloride reabsorption remained essentially constant until PNa exceeded 170 to 180 mM. At PNa 200 mM, sodium reabsorption was reduced by 22 ± 6%. In six other dogs, mechanical variations of GFR showed that the inhibitory effects of hypematremia (PNa 199 ± 3 mM) were less pronounced at low GFR. After subsequent administration of acetazolamide (30 mg/kg body wt), only 20% of control bicarbonate reabsorption remained and glomerulotubular balance was completely abolished. Both hypematremia and acetazolamide inhibited NaHCO3 and NaCl reabsorption in a molar ratio of about 1:2, as in normonatremic dogs. Finally, experiments in six dogs showed that the inhibitory effects of hypematremia (PNa 213 ± 4 mM) were not altered by varying PCO2 and plasma pH. We conclude that hypematremia inhibits paracellular water and NaCl reabsorption in the proximal tubules by reducing the osmotic force caused by transcellular NaHCO3 reabsorption. A rise in PNa does not stimulate transcellular NaCl reabsorption during distal inhibition by ethacrynic acid

A computational model of ureteral peristalsis and an investigation into ureteral reflux.

The aim of this study is to create a computational model of the human ureteral system that accurately replicates the peristaltic movement of the ureter for a variety of physiological and pathological functions. The objectives of this research are met using our in-house fluid-structural dynamics code (CgLes-Y code). A realistic peristaltic motion of the ureter is modelled using a novel piecewise linear force model. The urodynamic responses are investigated under two conditions of a healthy and a depressed contraction force. A ureteral pressure during the contraction shows a very good agreement with corresponding clinical data. The results also show a dependency of the wall shear stresses on the contraction velocity and it confirms the presence of a high shear stress at the proximal part of the ureter. Additionally, it is shown that an inefficient lumen contraction can increase the possibility of a continuous reflux during the propagation of peristalsis

Kjøpekraftsparitet og den norske kronen

I denne oppgaven benytter vi oss av konkurransekursindeksen (KKI) og euro for å undersøke om relativ kjøpekraftsparitet gjelder mellom Norge og utvalgte handelspartnere i perioden 1999-2020. Innledningsvis presenterer vi det teoretiske rammeverket til kjøpekraftsparitet, som gir en forutsetning for å kunne undersøke og tolke om pariteten er gjeldende i de valgte tidsseriene. Videre benytter vi oss av tidligere empiri for å få innsikt i resultatene av arbeid på den norske kronen. Empirisk forskning peker oss i retning av å bruke oljepris i tillegg til prisdifferanse som langsiktige forklaringsvariabler på bevegelser i den nominelle valutakursen. I et eget datakapittel gjennomgår vi de utvalgte variablene og tidsseriene grafisk gjennom en deskriptiv tolkning. Vi observerer at norsk prisvekst har en høyere vekstrate sammenlignet med handelspartnerne i etterkant av 2013, samtidig som realvalutakursen ikke returnerer til sin likevekt. Disse observasjonene ga oss et innblikk i forventede økonometriske resultater. I den empiriske analysen gjennomførte vi først en enkel test for kjøpekraftsparitet ved å teste for stasjonaritet i realvalutakursen. Ikke overraskende resulterte testen med at vi ikke kunne forkaste hypotesen om en «random-walk». Vi benytter oss videre av en regresjonsanalyse av oljeprisen, prisdifferansen og de nominelle valutakursene. Resultatene for oljepriskoeffisienten samsvarer med tidligere empiri. Koeffisientene til prisdifferansene viste derimot betydelige avvik fra forventet testverdi. Ved bruk av en Engle og Granger kointegrasjonstest av feilleddet kunne vi ikke påvise et langsiktig kointegrert forhold mellom variablene. Den empiriske analysen kunne ikke påvise relativ kjøpekraftsparitet mellom Norge og utvalgte handelspartnere i perioden 1999m2 til 2020m11. Avslutningsvis viser vi til lav prisvekstdifferanse, eksogene sjokk, utelatte kortsiktige forklaringsvariabler, bruk av månedlige observasjoner og et mulig strukturelt brudd i tidsserien, som potensielle årsaker til de svake testresultatene