In vitro online postdilution hemodiafiltration: effect ofvarious bicarbonate dialysis fluid concentrations on acid-base status

2009 ◽  
pp. 271-274
Author(s):  
H. Morel ◽  
M. Y. Jaffrin ◽  
P. Paullier ◽  
J. Vienken ◽  
C. Legallais
Keyword(s):  
Dialysis Fluid ◽  
Acid Base ◽  
Acid Base Status

Changes in uterine fluid composition and acid-base status during shell formation in the chicken

1989 ◽  
Vol 257 (4) ◽  
pp. R732-R737 ◽  
Author(s):  
Z. Arad ◽  
U. Eylath ◽  
M. Ginsburg ◽  
H. Eyal-Giladi
Keyword(s):  
Sharp Increase ◽  
Blood Gases ◽  
Future Application ◽  
Epithelial Tissue ◽  
Fluid Composition ◽  
Acid Base ◽  
Co2 Partial Pressure ◽  
Uterine Fluid ◽  
Acid Base Status

The aim of this study was to characterize the dynamic changes in uterine fluid composition and acid-base status during shell calcification in the chicken. Uterine eggs at timed intervals were manually aborted and the accompanying fluid collected and analyzed for composition of osmolytes, enzymes, and acid-base parameters. Blood samples were analyzed for comparison. No considerable change in blood gases took place in relation to residence time of the calcifying egg in the uterus. A significant acidosis occurred at latter stages. Only minor changes were revealed in plasma osmotic and biochemical composition throughout egg calcification. In contrast, major changes were revealed in uterine fluid composition and acid-base status during calcification. The most prominent phenomenon was the sharp increase in CO2 partial pressure, from 82.2 Torr at 0 h to 132.8 Torr at 10 h. As bicarbonate concentration remained almost stable, fluid pH dropped from 7.412 to 7.250 within this stage. Uterine fluid sodium and chloride concentrations and osmolality dropped significantly in the course of calcification, whereas potassium concentration significantly increased. A sharp increase in glucose, calcium, and magnesium concentrations was measured in the early stages of calcification. These findings are discussed in relation to existing models for transport mechanisms of the uterine epithelial tissue. The comprehensive picture that emerges from the present study should enable future application in establishing a self-contained culturing system in vitro for studies of embryonic development.

scholarly journals Management of pH of dialysis fluid using Carbostar directly effects the acid-base status in maintenance hemodialysis patients

2013 ◽  
Vol 46 (7) ◽  
pp. 651-659
Author(s):  
Motoyuki Masai ◽  
Takehiko Sakai ◽  
Junji Uchino ◽  
Atsushi Ishimaru ◽  
Toru Yamamoto ◽  
...  
Keyword(s):  
Hemodialysis Patients ◽  
Maintenance Hemodialysis ◽  
Dialysis Fluid ◽  
Acid Base ◽  
Acid Base Status ◽  
Maintenance Hemodialysis Patients

Cellular actions of cAMP on HCO3(-)-secreting cells of rabbit CCD: dependence on in vivo acid-base status

1994 ◽  
Vol 266 (4) ◽  
pp. F528-F535 ◽  
Author(s):  
C. Emmons ◽  
J. B. Stokes
Keyword(s):  
Anion Exchanger ◽  
Collecting Duct ◽  
Basolateral Membrane ◽  
Disulfonic Acid ◽  
Intercalated Cells ◽  
Cortical Collecting Duct ◽  
Acid Base ◽  
Acid Base Status

HCO3- secretion by cortical collecting duct (CCD) occurs via beta-intercalated cells. In vitro CCD HCO3- secretion is modulated by both the in vivo acid-base status of the animal and by adenosine 3',5'-cyclic monophosphate (cAMP). To investigate the mechanism of cAMP-induced HCO3- secretion, we measured intracellular pH (pHi) of individual beta-intercalated cells of CCDs dissected from alkali-loaded rabbits perfused in vitro. beta-Intercalated cells were identified by demonstrating the presence of an apical anion exchanger (cell alkalinization in response to removal of lumen Cl-). After 180 min of perfusion to permit decrease of endogenous cAMP, acute addition of 0.1 mM 8-bromo-cAMP or 1 microM isoproterenol to the bath caused a transient cellular alkalinization (> 0.20 pH units). In the symmetrical absence of either Na+, HCO3-, or Cl-, cAMP produced no change in pHi. Basolateral dihydrogen 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (0.1 mM) for 15 min before cAMP addition also prevented this alkalinization. In contrast to the response of cells from alkali-loaded rabbits, addition of basolateral cAMP to CCDs dissected from normal rabbits resulted in an acidification of beta-intercalated cells (approximately 0.20 pH units). The present studies demonstrate the importance of the in vivo acid-base status of the animal in the regulation of CCD HCO3- secretion by beta-intercalated cells. The results identify the possible existence of a previously unrecognized Na(+)-dependent Cl-/HCO3- exchanger on the basolateral membrane of beta-intercalated cells in alkali-loaded rabbits.

scholarly journals Temperature Effects on Haemolymph Acid-Base Status In Vivo and In Vitro in the Two-Striped Grasshopper Melanoplus Bivittatus

1988 ◽  
Vol 140 (1) ◽  
pp. 421-435 ◽  
Author(s):  
JON M. HARRISON
Keyword(s):  
Body Temperature ◽  
Carbonic Acid ◽  
Temperature Shift ◽  
Effect Of Temperature ◽  
Locomotory Activity ◽  
Acid Base ◽  
Protein Dissociation ◽  
Acid Base Status

In this study, I examine the effect of temperature on haemolymph acid-base status in vivo and in vitro in the two-striped grasshopper Melanoplus bivittatus. Melanoplus bivittatus experience wide (up to 40 °C) diurnal body temperature fluctuations in the field, but maintain body temperature relatively constant during sunny days by behavioural thermoregulation. Haemolymph pH was statistically constant (7.12) between 10 and 25°C, but decreased by −0.017 units °C− from 25 to 40°C. Relative alkalinity and fractional protein dissociation were conserved only at body temperatures at which feeding and locomotory activity occur, above 20°C. Haemolymph total CO2 (Ctot) increased from 10 to 20°C and decreased from 20 to 40°C. Haemolymph Pco2 increased from 10 to 20°C and was statistically constant between 20 and 40°C. Carbonic acid pKapp in haemolymph was 6.122 at 35°C, and decreased with temperature by −0.0081 units°C−1. Haemolymph buffer value averaged −35mequivl−1pHunit−1. Haemolymph pH changes with temperature were small (less than −0.004 units°C−1) in vitro at constant Pco2. Therefore, passive physicochemical effects cannot account for the pattern of acid-base regulation in vivo. The temperature shift from 10 to 20°C was accompanied by a net addition of 4.2-6.2 mmoll−1 of bicarbonate equivalents to the haemolymph. The temperature shift from 20 to 40°C was accompanied by a net removal of 10–14 mmoll−1 of bicarbonate equivalents from the haemolymph. Haemolymph acid-base regulation in vivo during temperature changes is dominated by active variation of bicarbonate equivalents rather than by changes in Pco2 as observed for most other air-breathers.

scholarly journals The effects of prolonged epinephrine infusion on the physiology of the rainbow trout, Salmo gairdneri. I. Blood respiratory, acid-base and ionic states

1987 ◽  
Vol 128 (1) ◽  
pp. 235-253 ◽  
Author(s):  
S. I. Perry ◽  
M. G. Vermette
Keyword(s):  
Rainbow Trout ◽  
Respiratory Acidosis ◽  
Salmo Gairdneri ◽  
Acid Base ◽  
Epinephrine Infusion ◽  
Extracellular Acidosis ◽  
Blood Ph ◽  
Acid Base Status ◽  
Ionic States

Rainbow trout were infused continuously for 24 h with epinephrine in order to elevate circulating levels of this hormone to those measured during periods of acute extracellular acidosis (approximately 5 X 10(−8) mol l-1). Concomitant effects on selected blood respiratory acid-base and ionic variables were evaluated. Infusion of epinephrine caused a transient respiratory acidosis as a result of hypoventilation and/or inhibition of red blood cell (RBC) bicarbonate dehydration. The acidosis was regulated by gradual accumulation of plasma bicarbonate. Even though whole blood pH (pHe) was depressed by 0.16 units, RBC pH (pHi) remained constant, thereby causing the transmembrane pH gradient (pHe-pHi) to decrease. A similar effect of epinephrine on RBC pH was observed in vitro, although the response required a higher concentration of epinephrine (2.0 X 10(−7) mol l-1). We speculate that the release of epinephrine during periods of depressed blood pH is important for preventing excessive shifts in RBC pH and for initiating a series of responses leading to plasma HCO3- accumulation and eventual restoration of blood acid-base status.

Stimulation of chloride transport by HCO3-CO2 in rabbit cortical collecting tubule

1986 ◽  
Vol 251 (1) ◽  
pp. F49-F56 ◽  
Author(s):  
K. Tago ◽  
V. L. Schuster ◽  
J. B. Stokes
Keyword(s):  
Chloride Transport ◽  
Acid Base ◽  
Cl Transport ◽  
Collecting Tubule ◽  
Acid Base Status ◽  
Stimulation Of ◽  
Rabbit Cortical Collecting Tubule ◽  
Cortical Collecting Tubule

We examined both the role of HCO3-CO2 in Cl transport as well as the effect of in vivo acid-base status on Cl transport by the rabbit cortical collecting tubule. The lumen-to-bath 36Cl tracer flux, expressed as the rate coefficient KCl, was measured in either HEPES-buffered (CO2-free) or HCO3-CO2-containing solutions. Amiloride was added to the perfusate to minimize the transepithelial voltage and thus the electrical driving force for Cl diffusion. Because KCl fell spontaneously with time in HCO3-CO2 solutions in the absence but not the presence of cAMP, we used cAMP throughout to avoid time-dependent changes. Acute in vitro removal of bath HCO3-CO2 reduced KCl. Acetazolamide addition in HEPES-buffered solutions also lowered KCl; KCl could be restored to control values by adding exogenous HCO3-CO2 in the presence of acetazolamide. In vivo acid-base effects on Cl transport were determined by dissecting tubules from either NaHCO3-loaded or NH4Cl-loaded rabbits. Tubules from HCO3-loaded rabbits had higher rates of Cl self exchange. Acute in vitro addition of bath HCO3-CO2 increased KCl and did so to a greater degree in tubules from HCO3-loaded rabbits. Most of this effect of HCO3-CO2 addition on KCl could not be accounted for by Cl-HCO3 exchange; rather, it appeared due to stimulation of Cl self exchange. The data are consistent with 36Cl transport occurring via Cl-HCO3 exchange as well as Cl self exchange. Both processes are acutely stimulated by HCO3 and/or Co2, and both are chronically regulated by in vivo acid-base status.

Effect of temperature on intracellular pH in crayfish neurons and muscle fibers

1984 ◽  
Vol 246 (1) ◽  
pp. C45-C49 ◽  
Author(s):  
J. L. Rodeau
Keyword(s):  
Intracellular Ph ◽  
Muscle Fibers ◽  
Effect Of Temperature ◽  
Cellular Regulation ◽  
Acid Base ◽  
Astacus Leptodactylus ◽  
Acid Base Status ◽  
Effects Of Temperature ◽  
Ph Microelectrodes

Intracellular pH microelectrodes were used to determine the effects of temperature (13-26 degrees C) on the in vitro regulation of intracellular acid-base status of neurons and muscle fibers of the crayfish Astacus leptodactylus. The values of the temperature coefficients delta pH/delta T (pH unit/degrees C) were -0.019 and -0.026 for muscles and neurons, respectively, values which are close to the temperature coefficient (-0.019) of the pK' of protein imidazole buffer groups. When temperature varies, the dissociation ratio of imidazole groups is thus maintained by the cellular regulation of cytoplasmic pH. According to the alphastat regulation hypothesis, this constancy would minimize the temperature effects on enzymic systems.

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