Changes in the plasma sodium concentration after minor, moderate and major surgery.

The plasma sodium concentration, [Na]P, falls following major surgery and this fall is exacerbated by the administration of sodium-free or sodium-low intravenous fluids in the postoperative period. As a prelude to prospective, but controlled, studies we observed the range of [Na]P on admission for surgery in 477 patients. In 309 patients the extent of the change in [Na]P by the first postoperative day (delta [Na]) was related to the severity of the operation undergone (minor, moderate or major) and the volume of potentially hypo-osmolar intravenous fluid given. The mean admission [Na]P was significantly lower with increasing severity of proposed operation. A highly significant fall occurred in [Na]P following surgery of every grade; such falls in [Na]P were seen even when no potentially hypo-osmolar fluids were administered. A significant inverse relationship between admission [Na]P and delta [Na] was demonstrated. We conclude that [Na]P falls following surgery of any severity and that such falls occur even when exogenous dilution cannot be implicated as a cause.

pK1' and bicarbonate concentration in plasma.

Values for pK1' were determined from pH measured at 37 degrees C with three blood-gas analyzers and from calculated pco2 values in 443 freshly separated plasmas, tonometered at 37 degrees C. Plasma was taken from healthy volunteers, seriously ill patients, and hyponatremic patients. pK1' values varied by considerably more than 0.06 in healthy volunteers as well as in very ill patients, and bicarbonate concentrations ([HCO3]p) calculated by blood-gas analyzers based on the pK1' value of 6.1 could be in error by some +/- 60%. pK1' was similarly determined for tonometered (37 degrees C) replicate dilutions of plasma samples. By adding weighed amounts of dry NaCl and NaHCO3 to the diluted samples we increased the Na+ concentration to approximately 150 mmol/L and bicarbonate concentrations to values ranging from approximately 2.5 to approximately 52.5 mmol/L. pK1' values decreased when [HCO3]p was increased in dilutions of plasma kept at constant ionic strength. At any given [HCO3]p, pK1' values were higher at high than at low values of pco2.

Changes in plasma solutes after food.

In experiments on 8 healthy young male volunteers, the ingestion of a large meal was found to cause plasma osmolality to rise from 288.8 +/- 0.8 (mean +/- s.e. mean) to 295.6 +/- 0.9 mmol/kg at 4 hours (P less than 0.001). There was an accompanying rise in plasma sodium (Na) from 141.9 +/- 0.8 to 144.6 +/- 0.8 mmol/l, also at 4 hours (P less than 0.01), but little change in other plasma electrolytes. Serum total amino acids rose slightly, non-esterified fatty acid fell minimally and changes in blood glucose concentrations were unremarkable. Thirst was experienced at plasma osmolality of 294.8 +/- 0.7 mmol/kg. Repeating the experiment either without food, or with the salt content of the meal only, was without effect on plasma Na, other solutes or osmolality. Postprandial hypersomolality and hypernatraemia is probably due to movement of water from the vascular compartment to the gut, or into cells. Plasma osmolality is best measured in the fasting state.

Acute biochemical responses to moderate beer drinking.

The consequences of drinking six pints of beer (3.31) over three hours were investigated in six healthy men. The expected rise in plasma osmolality, fall in plasma vasopressin concentration, and increase in free water clearance occurred; these variables had returned to normal by nine hours. There was a small but significant fall in plasma concentrations of urea and creatinine accompanied by a rise in plasma potassium concentration. Serum activities of alkaline phosphatase, gamma-glutamyl transferase, creatinine kinase, and lactate dehydrogenase did not change, and there was no alcohol-induced hypoglycaemia. All subjects had a slight hangover, but none was fluid depleted. It is concluded that, apart from inducing changes in water balance, alcohol in this form causes remarkably little metabolic disturbance.

Variability in pK'1 of human plasma.

(1) Results were presented of an investigation of the relationship between ionic strength and PK'1 (negative logarithmic form of the apparent overall first dissociation constant of carbonic acid in plasma) in separated human plasma at constant PCO2. (2) Ionic strength was varied by adding dry NaCl to diluted aliquots of plasma from six healthy people and dry NaCl plus dry NaHCO3 to diluted aliquots of plasma from six other healthy people. pK'1 was determined from simultaneous measurements of pH and PCO2, and measurements of TCO2. Values for solubility factor for CO2 (s) were corrected for differences in plasma water and in Na concentration. All plasmas were equilibrated at 37 degrees C in a tonometer with a constant gas mixture (5% CO2, 12% O2, 83% N2). Precision of pK'1 determinations averaged 0.003. pK'1 was also determined on fresh undiluted healthy plasma, similarly tonometered. (3) We report (a) considerable variability in pK'1 of fresh undiluted healthy plasma (from 6.0197 to 6.1217); and also in extrapolated values for pK'1 at a notional zero ionic strength (6.179 to 6.325); (b) that variation in plasma ionic strength alters pK'1; (c) that change in plasma bicarbonate [HCO3]p can also change pK'1; (d) that change in pK'1, changes measured pH. (4) Implications are discussed.

Hyponatraemia and severity and outcome of myocardial infarction.

A total of 235 consecutive patients admitted to a coronary care unit were investigated for serum electrolyte and urea concentrations; activities of aspartate amino-transferase, lactate dehydrogenase, and lactate dehydrogenase isoenzymes; electrocardiographic changes; clinical state; and outcome. Hyponatraemia, hypochloraemia, and uraemia were common in patients with confirmed myocardial infarctions, the degree of infarction correlating well with all the above indices of severity. The day-to-day variability of plasma sodium, chloride, and potassium concentrations was often increased above normal. Disturbances were greater in patients given diuretics. It is concluded that plasma sodium concentration fall after infarction and that the extent and duration of the fall are indices of the severity of the infarction.

Removal of extracellular fluid from muscle: assessment of a method.

Controlled compression of mouse biceps brachii muscle caused only partial extrusion of an extracellular protein (125I-albumin) from the muscle. Concentrations of sodium and potassium in the expressed fluid at any stage of compression did not correspond with concentrations expected for extracellular fluid. This procedure, therefore, does not selectively remove extracellular fluid from muscle.

Changes in myocardial water and solutes after ischemia.

Myocardial ischemia was produced in six dogs by arterial occlusion. Tissue contents of H2O, Na, Ca, and amino acids increased; K and (in one dog) Mg decreased. Variability in composition increased. Cell changes were evaluated with a method of appraising variability in composition between biopsies, and calculated (in three dogs) using extracellular fluid (ECF) volumes measured with [60Co]EDTA. Cell contents of H2O, Na, Cl, Ca, amino acids, and the molar quantity of nondiffusible solutes increased. Contents of K, nondiffusible anions (epicardium only) and total ionic strength of cell fluid decreased. Clinical implications are discussed.

Measurement of extracellular fluid after acute myocardial infarction.

The volume of distribution of [60Co]EDTA in normal dog myocardium is slightly less than that calculated from tissue contents of H2O, Cl, K, and their extracellular fluid (ECF) concentrations subsuming a steady state across cell membranes. The volume of distribution of [3H-]sorbitol was substantially higher than the measured CoEDTA space. [60Co]EDTA can be measured in ischemic myocardium that remains perfused. Extraction of [60Co]EDTA and [3H-]sorbitol is incomplete from dried biopsies.

Effects of ouabain on sodium uptake by frog heart and skeletal muscle.

Effects of ouabain (10(-3)-10(-12) M) on frog heart and skeletal muscle net uptake of Na from a K-free Conway-Ringer solution at 0-2 degrees C were investigated. Under these circumstances Na pumps are inactive and fibers are gaining Na even without ouabain. Changes in K, H2O, and solids were also measured. Na gains and K losses were increased by ouabain at greater than 10(-6) and greater than 10(-7) M, respectively, and decreased in heart muscle at less than or equal to 10(-8) M. It is suggested that these effects are due to actions on membrane permeability. Implications for mechanisms of positive inotropic effect of glycosides and for treatment are discussed.