Weight gain between dialyses in diabetics: possible significance of raised intracellular sodium content.
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Body Weight↗
Biomedical subjects
L Poston
Publications and source records attributed to L Poston.
Chlorieuretic or natriuretic hormone.
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Chlorine↗
Studies on mineralocorticoid 'escape' in cirrhosis.
1. The mineralocorticoid 9 alpha-fluorohydrocortisone was given to 12 patients with cirrhosis without ascites. In seven an 'escape' from its sodium-retaining effects was observed, the other five continuing to retain sodium. 2. Changes in plasma renin activity (PRA) and inulin clearance (Cinulin) were used in the assessment of possible changes in the 'effective' extracellular fluid volume. PRA fell and Cinulin increased to a similar extent in each of the two groups of patients. The findings do not support the concept that the failure to show the mineralocorticoid escape in some patients with cirrhosis is due to a failure of expansion of the effective extracellular fluid volume. 3. Sodium reabsorption in the different segments of the nephron as estimated by clearance techniques under conditions of maximal water diuresis showed that the greatest changes to account for both mineralocorticoid escape and sodium retention were in the part of the nephron beyond the diluting segment.
Adult↗
Validation of "transit renography" for the determination of the intrarenal distribution of plasma flow: comparison with the microsphere method in the anaesthetized rabbit and pig.
1. The spectrum of transit times of sodium o-iodohippurate (Hippuran) through the kidney can be derived from an 131I- (or 123I-) labelled Hippuran renogram by deconvolution. In the rabbit and pig, as has previously been shown in man, the frequency distribution curve for the transit times was bimodal. Since the transit time is likely to be proportional to the nephron length, the area of the first mode is likely to represent plasma flow to the shorter outer cortical nephrons whereas the delayed mode represents flow to the long juxtamedullary nephrons. 2. This interpretation was tested by simultaneously comparing renography with the microsphere method of measuring intrarenal plasma flow distribution in 12 rabbits and two pigs with a variety of anaesthetics. A close agreement was found between both methods for the percentage of plasma flow distributed to the outer cortical nephrons, thus supporting the use of "transit renography" to determine the intrarenal distribution of plasma flow.
Anesthetics↗
A study in vitro of the sodium pump in fulminant hepatic failure.
1. The mechanism underlying the raised leucocyte sodium content in fulminant hepatic failure was studied by measurement of sodium fluxes, (Na+ + K+)-dependent adenosine triphosphatase activity, and leucocyte ATP content. 2. The rate constant for sodium efflux in the leucocytes was significantly reduced, and attributable to reduced activity of the enzyme (Na+ + K+)-ATPase. Leucocyte ATP content was not significantly different from that of control cells. 3. Incubation of cells from patients in the sera of normal subjects resulted in a reversal of these changes. Inhibition of the leucocyte sodium efflux rate constants and (Na+ +K+)-ATPase of normal cells was achieved by incubation in sera from patients. 4. We suggest that the raised sodium content of leucocytes in fulminant hepatic failure is attributable to a defective sodium pumping mechanism, possibly due to a circulating toxin.
Adenosine Triphosphate↗
Changes in the electrolyte content of leucocytes at different clinical stages of cirrhosis.
The intracellular sodium, potassium, and water content of isolated leucocytes was estimated in 47 patients with cirrhosis. The values for sodium showed a wide scatter. In patients without ascites the mean value was significantly increased but in those accumulating ascites it was normal, although often reduced in individual subjects. Reduced values were found in patients with hyponatraemia associated with end-stage cirrhosis and diuretic treatment. Changes in leucocyte water content closely followed those in sodium content. Leucocyte potassium content was normal except in patients accumulating ascites in whom it was significantly reduced, indicating whole body depletion, and this could be corrected by administration of spironolactone.
Adult↗
Intracellular electrolyte abnormalities in fulminant hepatic failure.
The sodium, potassium, and water content of peripheral blood leukocytes was determined in 30 patients with fulminant hepatic failure. Although values for potassium were reduced, statistically significant increases were found in sodium and water content. Serial studies showed that, with recovery of liver function, the leukocyte sodium content fell initially to below normal, with values subsequently returning to the normal range some weeks later. Leukocyte sodium content was inversely correlated to the plasma sodium concentration, suggesting that a shift of sodium into the intracellular compartment might contribute toward the hyponatremia that was found in many patients.
Hepatic Encephalopathy↗
Placental NAD(P)H oxidase mediated superoxide generation in early pregnancy.
Early placental development is characterised by rapid cell differentiation and migration, matrix remodelling and angiogenesis. The enzyme NAD(P)H oxidase is a major source of superoxide anions implicated in signalling pathways regulating these processes in other systems. It is also thought to be involved in oxygen sensing and regulation of the expression of antioxidant genes. We therefore investigated NAD(P)H oxidase activity in placental tissues in early pregnancy and at term, and correlated this with antioxidant capacity. We collected placental tissues from women undergoing termination of pregnancy (n=19; gestational age 11(+6)+/-1(+0) weeks), and those with elective caesarean section at term after uncomplicated pregnancy (n=15; gestational age 38(+6)+/-0(+4) weeks). Tissues were assayed for superoxide production, using lucigenin chemiluminescence, and three independent markers of antioxidant capacity. In human placentas from normal deliveries at term substantial basal NAD(P)H activity was present. Activity was almost threefold higher in early pregnancy (P<0.0001). This was paralleled by higher total antioxidant capacity (P<0.0001), tissue glutathione concentrations (P<0.01) and gluthathione S-transferase enzyme activity (P<0.05) when compared to corresponding term placental values. NAD(P)H oxidase mediated superoxide generation could be an important modulator of the antioxidant defence response in early pregnancy.
Antioxidants↗
Normal expression of cell adhesion molecules in placentae from women with systemic lupus erythematosus and the antiphospholipid syndrome.
Pregnant women with active systemic lupus erythematosus (SLE) and/or the antiphospholipid syndrome (APS) are prone to recurrent miscarriage, pre-eclampsia, intrauterine growth restriction and premature delivery. Placental dysfunction may account for these complications yet the mechanisms remain uncertain. Amongst these, an inflammatory response in the placental vasculature could play a role, involving recruitment of neutrophils and platelets and the increased endothelial expression of cell adhesion molecules (CAM), central to the recruitment process. The aim of this study was primarily to investigate CAM expression in the fetoplacental vasculature in women with SLE/APS. Circulating maternal concentrations of soluble CAM were also elucidated. There were no differences in CAM immunostaining in placentae from patients with SLE and/or APS compared with controls. In both patients and controls moderate immunostaining for the intercellular adhesion molecule-1 (ICAM-1) was observed in placental vascular endothelium and mild immunostaining was present in the placental villous stroma. Strong immunostaining for platelet endothelial CAM (PECAM) occured in the placental vascular endothelium whereas P-selectin was mildly expressed in the stem vessel endothelium only. Vascular CAM-1 (VCAM-1) and E-selectin were undetectable in either study or control placentae. In contrast, ICAM-1 and VCAM-1 but not E-selectin, as assessed by immunoassay (ELISA), were elevated in maternal serum from SLE/APS patients compared with controls. This study suggests that upregulation of CAM expression and subsequent activation of neutrophil and/or platelet activity within the placental villous tree is unlikely to be a mechanism by which the adverse pregnancy outcome arises in SLE/APS pregnancies. However, maternal endothelial cell activation (ECA) may play a more important role.
Adult↗
Relationships between pHi and tension in isolated rat mesenteric resistance arteries.
Investigations into the relationship between pHi and tension were carried out in rat mesenteric resistance arteries. Acute acidosis, induced by ammonium chloride pre-pulse, led to variable and transient tension development, but simultaneous removal of extracellular sodium led to a sustained rise in tension associated with maintained intracellular acidification. Dependence of tension and pHi recovery from acute acidosis on Na/H exchange and anion exchange pathways was demonstrated using pharmacological inhibitors. Additionally, removal of HCO3 suggested the anion pathway involved was Na-dependent HCO3 transport. Removal of extracellular calcium, or pharmacological inhibition of voltage-dependent calcium channels, prevented the tension development in response to NH4Cl pre-pulse in an Na-free medium, but did not affect pHi. Intracellular acidosis resulting from elevation of the PCO2 resulted in initial vasoconstriction followed by profound vasodilatation of arteries pre-contracted with noradrenaline (NA). The response to alkalosis induced by NH4Cl or by lowering the PCO2 led to initial dilatation followed by potentiation of NA-induced tension.
Ammonium Chloride↗
Effects of pH on vascular tension: which are the important mechanisms?
The pH has marked effects on the blood flow in several vascular beds but the underlying mechanisms remain incompletely understood. It is still not agreed, for example, whether it is the fall in extracellular pH or intracellular pH that is responsible for changes in tone resulting from hypercapnic acidosis. The issue has been further complicated by the recent discovery that nitric oxide (NO) may also be involved in vasodilator responses to hypercapnia with the result that, in some laboratories, attention has been focused away from vascular smooth muscle. The recent availability of fluorescent dyes sensitive to pH has enabled some of the uncertainties in this field to be addressed. In light of these new observations, we have attempted to put older viewpoints in perspective. We conclude that, whilst a fall in smooth muscle intracellular pH is likely to be responsible for immediate responses to acidosis, the extracellular pH probably plays the predominant role in the steady state. The role of NO is best investigated in the cerebral circulation where it plays an important modulating role in the response to acidosis, and is probably of extravascular origin.
Acidosis↗
Offspring of normal and diabetic rats fed saturated fat in pregnancy demonstrate vascular dysfunction.
BACKGROUND: Disturbances of the in utero environment may "program" for disease in later life. In this study, we determined whether dietary fat supplementation and/or diabetes in pregnancy can adversely affect vascular function in the offspring. METHODS AND RESULTS: Female Sprague-Dawley rats were fed a breeding diet or a diet high in saturated fat (30% wt/wt) for 10 days before mating, throughout pregnancy, and postpartum. Endothelium-dependent relaxation to acetylcholine was blunted in isolated femoral arteries of 15-day-old weanling pups from dams fed the 30%-fat diet. Endothelial dysfunction and enhanced constrictor responses to norepinephrine were also observed in an additional study of 60-day-old offspring of dams fed 20% saturated fat. Rats with streptozotocin-induced diabetes were also fed saturated fat during pregnancy. Femoral arteries from their 15-day-old offspring showed impairment of endothelium-dependent dilation and enhanced constrictor responses to norepinephrine and the thromboxane mimetic U46619 compared with young offspring of high-fat-fed normal dams. The 30%-fat diet was also deleterious to vascular function in the maternal diabetic animals when assessed in mesenteric arteries 16 days postpartum. CONCLUSIONS: A high-fat diet in pregnancy led to vascular dysfunction in rat weanlings and young adult offspring. Vascular function further deteriorated in weanlings if the maternal rat was diabetic.
Acetylcholine↗