Leucocyte Intracellular pH in Patients with the Metabolic Acidosis of Renal Failure

1977 ◽  
Vol 52 (3) ◽  
pp. 325-328 ◽  
Author(s):  
G. E. Levin ◽  
D. N. Baron
Keyword(s):  
Renal Failure ◽  
Metabolic Acidosis ◽  
Intracellular Ph ◽  
Healthy Subjects ◽  
Venous Blood ◽  
Ph Measurements ◽  
Made In

1. Human leucocytes were isolated from venous blood and resuspended in the subject's plasma. 2. Intracellular pH measurements were made in vitro by the dimethyloxazolidinedione technique in 13 healthy subjects and in 11 subjects with renal failure and metabolic acidosis. 3. The intracellular pH of the healthy subjects was found to be 7·07 (sd 0·04), significantly lower than that of the patients, which was 7·11 (sd 0·03). For all estimations plasma Pco2 was maintained at approximately 5·5 kPa. The methodological and possible metabolic reasons for this difference in intracellular pH are discussed.

The Intracellular pH of Human Leucocytes in Response to Acid—Base Changes in Vitro

1976 ◽  
Vol 50 (4) ◽  
pp. 293-299 ◽  
Author(s):  
G. E. Levin ◽  
P. Collinson ◽  
D. N. Baron
Keyword(s):  
Metabolic Acidosis ◽  
Intracellular Ph ◽  
Metabolic Alkalosis ◽  
Venous Blood ◽  
Bicarbonate Concentration ◽  
Acid Base ◽  
Ph Measurements

1. Viable human leucocytes were isolated from venous blood and suspended in artificial media. Intracellular pH measurements were made by the dimethyloxazolidinedione technique in conditions simulating ‘respiratory’ or ‘metabolic’ acid-base disturbances. 2. Normal intracellular pH was 7·11 ± 0·02 (mean ± 2 sd) at an extracellular Pco2 of 5·8 kPa and a bicarbonate concentration of 25 mmol/l. 3. ‘Respiratory’ and ‘metabolic’ acidosis caused little change in pH1 although increases in Pco2 led to relatively greater falls in pH1 than did reduction in external bicarbonate concentration. 4. ‘Respiratory’ and ‘metabolic’ alkalosis caused similar and relatively greater increases in the pH1 when compared with the response to an external acidosis.

Intracellular pH measurements in Kidney in vitro — New advantages on single cell diagnosis in the intact organ

2000 ◽  
Vol 118 (4) ◽  
pp. A1109
Author(s):  
Michael J. Sessler ◽  
Christina Baumstark ◽  
Joerg Weik ◽  
Michael Weinlich ◽  
Richard Viebahn ◽  
...  
Keyword(s):  
Single Cell ◽  
Intracellular Ph ◽  
Ph Measurements ◽  
Single Cell Diagnosis

Bicarbonate Therapy and Intracellular Acidosis

1997 ◽  
Vol 93 (6) ◽  
pp. 593-598 ◽  
Author(s):  
D. J. A. Goldsmith ◽  
L. G. Forni ◽  
P. J. Hilton
Keyword(s):  
Carbon Dioxide ◽  
Metabolic Acidosis ◽  
Sodium Bicarbonate ◽  
Intracellular Ph ◽  
Extracellular Fluid ◽  
Intracellular Acidification ◽  
Intracellular Acidosis ◽  
Bicarbonate Therapy ◽  
Intracellular Alkalinization

1. The correction of metabolic acidosis with sodium bicarbonate remains controversial. Experiments in vitro have suggested possible deleterious effects after alkalinization of the extracellular fluid. Disequilibrium of carbon dioxide and bicarbonate across cell membranes after alkali administration, leading to the phenomenon of ‘paradoxical’ intracellular acidosis, has been held responsible for some of these adverse effects. 2. Changes in intracellular pH in suspensions of leucocytes from healthy volunteers were monitored using a fluorescent intracellular dye. The effect in vitro of increasing extracellular pH with sodium bicarbonate was studied at different sodium bicarbonate concentrations. Lactic acid and propionic acid were added to the extracellular buffer to mimic conditions of metabolic acidosis. 3. The addition of a large bolus of sodium bicarbonate caused intracellular acidification as has been observed previously. The extent of the intracellular acidosis was dependent on several factors, being most evident at higher starting intracellular pH. When sodium bicarbonate was added as a series of small boluses the reduction in intracellular pH was small. Under conditions of initial acidosis this was rapidly followed by intracellular alkalinization. 4. Although intracellular acidification occurs after addition of sodium bicarbonate to a suspension of human leucocytes in vitro, the effect is minimal when the conditions approximate those seen in clinical practice. We suggest that the observed small and transient lowering of intracellular pH is insufficient grounds in itself to abandon the use of sodium bicarbonate in human acidosis.

scholarly journals Comparative Study of the Cellular Pharmacodynamics of Calcineurin Inhibitors between Patients with Chronic Renal Failure Awaiting Renal Transplantation and Cirrhosis Patients Awaiting Liver Transplantation

2009 ◽  
Vol 18 (5-6) ◽  
pp. 639-646 ◽  
Author(s):  
Yu Kihara ◽  
Naoto Matsuno ◽  
Abuduxukuer Mijiti ◽  
Takeshi Nagao ◽  
Hironori Takeuchi ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Renal Failure ◽  
Renal Transplantation ◽  
Chronic Renal Failure ◽  
Mononuclear Cells ◽  
Venous Blood ◽  
Calcineurin Inhibitors ◽  
Peripheral Blood Mononuclear ◽  
Drug Concentrations

The in vitro response of peripheral blood mononuclear cells (PBMCs) to the suppressive effects of calcineurin inhibitors is known to correlate with the clinical efficacy of drugs used in renal transplantations. The present study was conducted to examine the differences of PBMC responses to calcineurin inhibitors between chronic renal failure (CRF) patients awaiting renal transplantation and cirrhosis patients awaiting liver transplantation. The study included 99 CRF patients awaiting renal transplantation and 27 cirrhosis patients awaiting liver transplantation. Twenty milliliters of venous blood was taken 1–7 days before transplantation. The in vitro drug concentrations giving 50% inhibition of PBMC blastogenesis stimulated with concanavalin A (IC50s) were calculated. The suppressive effects of tacrolimus against PBMC blastogenesis were more than 10–100 times stronger than those of cyclosporine. The median IC50 value for cyclosporine against the CRF PBMCs was not significantly different from the median IC50 value against the cirrhosis PBMCs. In contrast, tacrolimus sensitivity in cirrhosis PBMCs is approximately seven times higher than that in CRF PBMCs. The median IC50 value for tacrolimus against cirrhosis PBMCs was significantly lower and therefore the effect was stronger in comparison to the CRF PBMCs ( p < 0.001). These data suggest that the PBMCs of cirrhosis patients, in comparison to those of CRF patients, are highly sensitive to the suppressive effect of tacrolimus. However, PBMC sensitivity to cyclosporine was not significantly different between the CRF and cirrhosis patients. These observations raise the possibility that treatment with tacrolimus, rather than cyclosporine, may therefore be a better choice to reduce the risks of allograft rejection in liver transplantation.

scholarly journals Effect of (1→3),(1→6)-β-Glucan on In Vitro Production of Cytokines by Leukocytes of Patients With Periodontitis

Medicina ◽  
2012 ◽  
Vol 48 (4) ◽  
pp. 27
Author(s):  
Laimis Akramas ◽  
Dalia Akramienė ◽  
Jurgina Sakalauskienė ◽  
Ričardas Kubilius ◽  
Alvydas Gleiznys
Keyword(s):  
Periodontal Disease ◽  
Healthy Subjects ◽  
Venous Blood ◽  
In Vitro Study ◽  
Interleukin 10 ◽  
Control Group ◽  
In Vitro Production ◽  
Blood Leukocytes ◽  
Tnf Α

Background. The aim of the study was to investigate the effect of (1→3), (1→6)-β-glucan on the production of interleukin 10 (IL-10) and tumor necrosis factor α (TNF-α) in vitro by peripheral blood leukocytes of patients with periodontitis. Material and Methods. In total, 20 patients suffering from untreated severe chronic generalized periodontitis were enrolled in this study. Periodontitis was confirmed by clinical and radiologic examination. Besides, 20 periodontally healthy patients served as a control group. Peripheral venous blood was sampled from the patients, and isolated leukocytes were treated with (1→3),(1→6)-β-glucan from yeast at different concentrations. The levels of IL-10 and TNF-α secreted by the leukocytes unstimulated and stimulated with unopsonized E. coli in vitro were determined by the enzyme amplified sensitivity immunoassay method. Results. Our data showed that (1→3),(1→6)-β-glucan induced a significant decrease (P<0.05) in the TNF-α level and a significant increase (P<0.001) in the IL-10 level in the media of unstimulated and stimulated leukocytes of the patients with periodontitis in comparison with those of the healthy subjects. Conclusions. The present in vitro study showed that (1→3),(1→6)-β-glucan modulated the response of leukocytes of the patients with periodontitis differently in comparison with those of the healthy subjects. It increased the release of IL-10, which is protective of the tooth-supporting tissues in patients with periodontal disease, but decreased the release of TNF-α, which is mainly responsible for the destruction of the tooth-supporting tissues during periodontal disease.

Methods for detecting local intestinal ischemic anaerobic metabolic acidosis by P CO 2

1996 ◽  
Vol 81 (4) ◽  
pp. 1834-1842 ◽  
Author(s):  
Ranna A. Rozenfeld ◽  
Michael K. Dishart ◽  
Tor Inge Tønnessen ◽  
Robert Schlichtig
Keyword(s):  
Blood Flow ◽  
Metabolic Acidosis ◽  
Anaerobic Threshold ◽  
In Vitro Model ◽  
Venous Blood ◽  
Flow Reduction ◽  
Portal Venous Blood ◽  
Vitro Model ◽  
Arterial Plasma

Rozenfeld, Ranna A., Michael K. Dishart, Tor Inge Tønnessen, and Robert Schlichtig. Methods for detecting local intestinal ischemic anaerobic metabolic acidosis by[Formula: see text]. J. Appl. Physiol. 81(4): 1834–1842, 1996.—Gut ischemia is often assessed by computing an imaginary tissue interstitial pH from arterial plasma [Formula: see text] and the[Formula: see text] in a saline-filled balloon tonometer after equilibration with tissue[Formula: see text](P[Formula: see text]). P[Formula: see text] may alternatively be assumed equal to venous[Formula: see text]([Formula: see text]) in that region of gut. The idea is that as blood flow decreases, gut P[Formula: see text] and[Formula: see text] will increase to the maximum aerobic value, i.e., maximum respiratory[Formula: see text]([Formula: see text]). Above a “critical” anaerobic threshold, lactate (La−) generation, by titration of tissue [Formula: see text], should raise P[Formula: see text]above[Formula: see text]. During progressive selective whole intestinal flow reduction in six pentobarbital-anesthetized pigs, we used[Formula: see text] electrodes to test the hypotheses that critical P[Formula: see text]is achieved earlier in mucosa than in serosa and that[Formula: see text], computed using an in vitro model, predicts critical P[Formula: see text]. We defined critical P[Formula: see text] as the inflection of P[Formula: see text]-[Formula: see text]vs. O2 delivery (Q˙o 2) plots. CriticalQ˙o 2for O2 uptake was 12.55 ± 2 ml ⋅ kg−1 ⋅ min−1. Critical P[Formula: see text] for mucosa and serosa was achieved at similar whole intestineQ˙o 2(13.90 ± 5 and 13.36 ± 5 ml ⋅ kg−1 ⋅ min−1, P = NS). Critical P[Formula: see text] (129 ± 24 and 96 ± 21 Torr) exceeded[Formula: see text](62 ± 3 Torr). During ischemia, La− excretion into portal venous blood was matched by K+excretion, causing [Formula: see text] to increase only slightly, despite P[Formula: see text] rising to 380 ± 46 (mucosa) and 280 ± 38 (serosa) Torr. These results suggest that mucosa and serosa become dysoxic simultaneously, that ischemic dysoxic gut is essentially unperfused, and that in vitro predicted[Formula: see text]underestimates critical P[Formula: see text].

ADRENOCORTICAL FUNCTION IN RATS AFTER LESION OF THE PITUITARY STALK

1962 ◽  
Vol 25 (1) ◽  
pp. 9-18 ◽  
Author(s):  
K. KOVÁCS ◽  
MARGIT A. DÁVID ◽  
F. A. LÁSZLÓ
Keyword(s):  
Functional Capacity ◽  
Adrenal Glands ◽  
Venous Blood ◽  
Pituitary Stalk ◽  
Adrenocortical Function ◽  
Histological Structure ◽  
Unilateral Adrenalectomy ◽  
And Control ◽  
Made In

SUMMARY Lesions were made in the pituitary stalk of rats, and the functional capacity of the hypophysial-adrenocortical axis of animals suffering from diabetes insipidus was studied. Eight days after the operation the weight, histological structure and histologically demonstrated lipid content of the adrenals had not changed. Whereas operative stress and unilateral adrenalectomy caused no ascorbic acid depletion in the contralateral adrenals, administration of adrenocorticotrophic hormone induced a significant decrease. The corticosterone content of the adrenal venous blood decreased moderately, whilst in vitro the adrenal slices secreted less corticosterone than normally. Secretion of aldosterone by the adrenals of animals with lesions was not different from that of controls. When large doses of corticosterone were administered adrenal atrophy occurred in both operated and control rats. It is concluded that the functional capacity of the hypophysial—adrenocortical axis is decreased 8 days after the destruction of the pituitary stalk, although the production of hormones by the adrenal cortex does not cease completely; one must be cautious in assessing the functional state of the adrenal glands since the methods used for their evaluation do not always give comparable results.

scholarly journals Can Venous Blood Gases Replace Arterial Blood Gases in Diabetic Ketoacidosis/Renal Failure Induced Metabolic Acidosis?

2015 ◽  
Vol 3 (3) ◽  
pp. 65-69
Author(s):  
Naveen Mohan ◽  
Gireesh Kumar K. P ◽  
Sreekrishnan T. P ◽  
Ajith Kumar J ◽  
Ajith V. ◽  
...  
Keyword(s):  
Renal Failure ◽  
Metabolic Acidosis ◽  
Diabetic Ketoacidosis ◽  
Venous Blood ◽  
Blood Gases ◽  
Arterial Blood Gases ◽  
Arterial Blood

Determination of liver intracellular pH in vivo and its homeostasis in acute acidosis and alkalosis

1979 ◽  
Vol 236 (3) ◽  
pp. F240-F245 ◽  
Author(s):  
R. Park ◽  
W. J. Leach ◽  
A. I. Arieff
Keyword(s):  
Metabolic Acidosis ◽  
Intracellular Ph ◽  
Venous Blood ◽  
Respiratory Acidosis ◽  
Normal Liver ◽  
Respiratory Alkalosis ◽  
Arterial Blood ◽  
Acute Metabolic Acidosis

An in vivo method is presented for the determination of liver intracellular pH (pHi) using [14C]dimethadione (DMO) in dogs. This method differs from those previously published in that hepatic venous and portal venous blood pH were selected as the extracellular reference pH, and liver blood space corrections are applied to whole liver tissue [14C]DMO activity. Using these corrections, a normal liver pHi of 6.99 +/- 0.03 (SE) was obtained. During acute metabolic acidosis and alkalosis, as well as during acute respiratory acidosis and alkalosis, the liver pHi remained normal; metabolic acidosis was 7.04 +/- 0.04; metabolic alkalosis was 6.92 +/- 0.08; respiratory acidosis was 6.98 +/- 0.04; and respiratory alkalosis was 7.00 +/- 0.10. None of these values was significantly different from normal (P greater than 0.05). Changes in intracellular bicarbonate and lactate appeared to account in part for the observed stability of the liver pHi despite acute manipulations resulting in a range of pH values between 7.09 and 7.63 in arterial blood.

scholarly journals Effect of an acute oral protein load on renal acidification in healthy humans and in patients with chronic renal failure.

1997 ◽  
Vol 8 (5) ◽  
pp. 784-792
Author(s):  
N G de Santo ◽  
G Capasso ◽  
G Malnic ◽  
P Anastasio ◽  
L Spitali ◽  
...  
Keyword(s):  
Renal Failure ◽  
Metabolic Acidosis ◽  
Chronic Renal Failure ◽  
Urinary Excretion ◽  
Healthy Subjects ◽  
Tubular Reabsorption ◽  
Renal Tubules ◽  
Acid Base Balance ◽  
Acid Base ◽  
Base Balance

The effect of a meat load on the renal handling of acid-base balance was studied in ten healthy subjects (GFR by inulin clearance = 98.5 +/- 8.14 ml.min-1.1.73 m-2) and in ten patients affected by chronic renal failure (CRF) (GFR = 39.9 +/- 5.3 ml.min-1.1.73 m-2). After the meat load (2 g.kg-1 body weight of cooked unsalted red meat), GFR increased by 26.9% (peak value) over baseline in healthy subjects and by 32% in CRF patients. The acid-base status of the healthy subjects was in the normal range, whereas the CRF patients disclosed a slight metabolic acidosis. After a meat load, there was, in the healthy subjects, an increase in the filtered load of bicarbonate coupled to an enhanced tubular reabsorption and urinary excretion. The time course between bicarbonate load and urinary excretion was coincident. In CRF patients, the increase of bicarbonate tubular load after the meal was associated with an increase in tubular reabsorption but not in urinary excretion of this anion. The relationship between bicarbonate load and reabsorption was linear in both groups up to the highest filtered loads. Baseline titratable acidity (TA) and ammonium (NH4+) excretion (expressed per ml GFR) were increased in CRF patients as compared with control subjects, but no changes were found after the meat load in both groups in these experimental conditions. The data indicate that the renal tubules contribute to the maintenance of acid-base balance both in healthy subjects and in CRF patients by reabsorbing most of the additional bicarbonate load. The transient, but significant, increase in bicarbonate excretion observed in healthy subjects could be related to the increased tubular load of bicarbonate. In CRF patients, tubular bicarbonate reabsorption was more complete, possibly because of the stimulation of H+ secretion by the mild metabolic acidosis. TA and NH4+ did not participate in tubular compensation of the increased buffer load.

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