The Mechanism of Acidosis Produced by Hyperosmotic Infusions*

Winters, Robert W.; Scaglione, Peter R.; Nahas, Gabriel G.; Verosky, Maryagnes

doi:10.1172/jci104950

Cited by 70 publications

(16 citation statements)

References 17 publications

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“…No measurements of the acid-baSe status of the volunters were performed in this study. However, the significant decrease in [(SNa + SK)--Sc~] points to a decrease in HCO 3 induced by saline infusion in agreement with the concept of "dilution acidosis" [4,5,12,16,21]. Also, in the present study hypertonic saline infusion was associated with marked changes in serum calcium and plasma renin activity.…”

Section: Discussionsupporting

confidence: 90%

“…Hypertonic saline infusion into nephrectomized dogs mechanically ventilated with pCO 2 held constant has been shown to induce a fall in plasma bici~rbonate and pH [12,21]. Since infusion of hypertonic mannitol was followed by a comparable degree of extracellular acidosis a role of extracellular Na + in the mechanism of extracellular acidification in this Setting can be excluded.…”

Section: Discussionmentioning

confidence: 99%

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Hypertonic saline infusion induces activation of the lymphocyte Na+/H+ antiport and cytosolic alkalinization in healthy human subjects

et al. 1994

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The Na+/H+ antiport is a membrane transport protein that extrudes intracellular protons in exchange for extracellular sodium. Some details of its physiological and pathophysiological role remain poorly defined. Experimental evidence suggests that the antiporter is involved in the regulation of cell volume. In the present study, we therefore investigated the activity of the lymphocyte Na+/H+ antiport in nine healthy volunteers following acute hypertonic (2.5%) saline infusion (4 mmol NaCl/kg over 120 min). Antiport activity was measured after acidifying the cells with Na+ propionate (5-40 mM) using the fluorescent dye bis-carboxyethyl carboxyfluorescein. Hypertonic saline induced significant increases in plasma osmolality (308.4 +/- 2.3 vs. 293.5 +/- 2.7 mOsm/kg; P < 0.01), serum Na+ (150.8 +/- 3.7 vs. 138.9 +/- 0.5 mmol/kg; P < 0.01), and Cl- concentrations (118.0 +/- 3.9 vs. 101.1 +/- 1.0 mmol/kg; P < 0.01). Extracellular hypertonicity was followed by a stimulated activity of the lymphocyte Na+/H+ antiport with an increase in the apparent Vmax values from 2.44 +/- 0.16 to 3.27 +/- 0.34 10(-3) s-1 (P < 0.01) and a slight rise in pK, from 6.81 +/- 0.03 to 6.87 +/- 0.03 (P < 0.05) after hypertonic saline. In addition to antiport activation, cytosolic alkalinization was observed with cytosolic pH values averaging 6.90 +/- 0.02 before and 6.99 +/- 0.02 (P < 0.01) after hypertonic saline. Our results show for the first time that acute extracellular hypertonicity in man due to hypertonic NaCl loading is associated with a stimulated lymphocyte Na+/H+ antiport activity and cytosolic alkalinization.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 99%

Hypertonic saline infusion induces activation of the lymphocyte Na+/H+ antiport and cytosolic alkalinization in healthy human subjects

et al. 1994

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“…. Correction of DKA or hypertonic dilution acidosis [43] may have minor hypokalemic effects. The effects of factors not related to DH or insulin can be variable.…”

Section: Summary Of Insulin Actions: Applications To Other Examples Omentioning

confidence: 99%

Abnormalities of serum potassium concentration in dialysis-associated hyperglycemia and their correction with insulin: a unique clinical/physiologic exercise in internal potassium balance

Tzamaloukas

Ing²,

Elisaf

et al. 2010

Int Urol Nephrol

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The absence of significant losses of potassium in the urine makes dialysis-associated hyperglycemia (DH) a model for the study of the internal potassium balance. Studies of DH have revealed that hyperkalemia is frequent at presentation, insulin infusion is usually the only treatment required, and the magnitude of the decrease in serum potassium concentration (K(+)) during treatment of DH with insulin depends on the starting serum K(+) level, the decreases in serum glucose concentration and tonicity, and the increase in serum total carbon dioxide level. We present an analysis of these findings based on previously studied actions of insulin. Calculations of transcellular potassium shifts based on the combined effects of insulin-the increase in the electrical potential differences (hyperpolarization) of the cell membranes and the correction of the hyperglycemic intracellular dehydration through decrease in serum glucose concentration-produced quantitative predictions of the decrease in serum K(+) similar to the reported changes in serum K(+) during treatment of DH with insulin. The lessons from analyzing serum K(+) changes during treatment of DH with insulin are applicable to other conditions where internal potassium balance is called upon to protect serum K(+), such as the postprandial state. The main questions related to internal potassium balance in DH that await clarification include the structure and function of cell membrane potassium channels, the effect of insulin on these channels, and the mechanisms of feedforward potassium regulation.

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“…The expansion of the extracellular volume is known to cause a decrease in bicarbonate and sodium reabsorption in the proximal renal tubules (Winters et al, 1959;Purkerson et al, 1969;Kurtz man, 1970;Moore et al, 1972) which is accompanied by an increased flux of H+ from the tubular lumen into body fluids. The reverse of events can be induced by the contraction of the extracel lular volume.…”

Section: Discussionmentioning

confidence: 99%

Plasma Osmolality in the Early and Late Neonatal Period with Particular Reference to Low Birth Weight Infants

Mestyán¹,

Horváth²,

Mestyán³

1976

Neonatology

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Data on postnatal changes of plasma osmolality were collected on two groups of newborn infants. Group I consisted of 114 normal full-term infants in whom measurements were performed in cord blood and peripheral venous blood at 12, 24 and 48 h after birth. It has been found that plasma osmolality does not change within the first 48 h, but is maintained at the level of cord plasma. The infants comprising group II were admitted to a referral unit at different postnatal ages for observation or treatment of transient neonatal disturbances. The majority of the infants and particularly those followed through the late neonatal period were low birth weight infants. Neither of the infants studied required intravenous therapy known to affect plasma osmolality. Blood samples were taken at admission and at different time intervals thereafter. Time at which blood was withdrawn varied in the individual infant. In 95 plasma samples, besides osmolality, sodium concentration was also measured. In this group of infants, after the first 3 days, plasma osmolality steadily fell with postnatal age reaching a minimum between 18–21 days. The fall in plasma osmolality was accompanied by a parallel decline of plasma sodium. The two variables were significantly correlated. It is concluded that the decrease in plasma osmolality of low birth weight infants represents profound adaptive changes of osmolal homeostasis in the late neonatal period. The possible mechanisms underlying the total osmotic pressure changes, such as expansion of extracellular volume, sodium loss, immaturity of kidney function are discussed.

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The Mechanism of Acidosis Produced by Hyperosmotic Infusions*

Cited by 70 publications

References 17 publications

Hypertonic saline infusion induces activation of the lymphocyte Na+/H+ antiport and cytosolic alkalinization in healthy human subjects

Hypertonic saline infusion induces activation of the lymphocyte Na+/H+ antiport and cytosolic alkalinization in healthy human subjects

Abnormalities of serum potassium concentration in dialysis-associated hyperglycemia and their correction with insulin: a unique clinical/physiologic exercise in internal potassium balance

Plasma Osmolality in the Early and Late Neonatal Period with Particular Reference to Low Birth Weight Infants

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