Biomedical subjects
H J Carroll
Publications and source records attributed to H J Carroll.
Osmometry of CO2 in gas samples.
Measurement of solute concentrations in biologic fluids by an osmometric technique has been described previously. Here, we describe an osmometric technique for measuring CO2 in gas samples. A solution of NaOH is injected into a graduated syringe containing the gas sample and CO2 is trapped in the reaction: 2NaOH + CO2 leads to Na2CO3 + H2O. The decrease in osmolality of the NaOH solution allows estimation of pCO2 in the original gas sample.
Pseudohypoaldosteronism following kidney transplantation.
A 56-year-old woman received a kidney transplant and presented subsequently with evidence of volume contraction, hyponatremia and hyperkalemia. Urinary sodium excretion was inappropriately high for the degree of volume contraction and urinary potassium excretion inappropriately low for the degree of hyperkalemia. Marked elevation of plasma renin activity and plasma aldosterone suggested that the renal tubules were unresponsive to mineralocorticoids. The defect was shown to be transient. The mechanisms leading to the defect are discussed.
The mechanism of hyperchloremic acidosis during the recovery phase of diabetic ketoacidosis.
To determine the mechanism of hyperchloremic acidosis during recovery from diabetic ketoacidosis (DKA), serial measurements were made in eight patients of serum and urinary electrolytes and organic acids, and of urinary net acid. On admission, the average decrease in serum total CO2 was 17.5 mmol/L, corresponding to the excess anion gap, 18.5 meq/L, and the serum organic acids, 17.1 meq/L. With the treatment, the anion gap and organic acids decreased by 16.1 and 14.7 meq/L, respectively, but the serum CO2 increased only by 8.4 mmol/L; serum electrolyte balance was maintained by increase in chloride concentration. Fluid retention was insufficient to explain the disparity between the increase in CO2 and the decrease in organic acids. Renal loss of bicarbonate precursors during treatment was modest and was exceeded by renal bicarbonate production. The disparity between the increase in serum CO2 and the decrease in organic acids during treatment of DKA may be explained to a large extent by a difference in volume of distribution between bicarbonate and organic anions. The renal loss of ketone anions before admission, however, is ultimately responsible for the persistence of substantial metabolic acidosis.
Pathophysiology of the syndrome of hyporeninemic hypoaldosteronism.
Explore the source record for details and available documents.
Heparin-induced hyperkalemia: report of a case.
A 77-year-old diabetic man with a creatinine clearance of 23--27 ml/min developed hyperkalemia while receiving heparin for peripheral arterial insufficiency. Discontinuation of this agent led to resolution of hyperkalemia as the plasma aldosterone concentration multiplied by sixfold. Renal insufficiency may have predisposed this patient to the development of hyperkalemia when heparin therapy suppressed aldosterone synthesis.
D-lactic acidosis in a man with the short-bowel syndrome.
Explore the source record for details and available documents.
Determination of urinary ammonia by osmometry.
Explore the source record for details and available documents.
Consumpton of CO2 in metabolism of acetate as an explanation for hypoventilation and hypoxemia during hemodialysis.
Explore the source record for details and available documents.
The renin-aldosterone system and thiazide-induced depletion of total body potassium in essential hypertension.
15 patients who had benign, uncomplicated essential hypertension, were treated with chlorthiazide (500 mg twice a day) with or without propranolol (10--20 mg 4 times a day), and the effect of the treatment on plasma renin activity (PRA), urinary aldosterone excretion, total body potassium (TBK) and plasma sodium and potassium was evaluated. TBK depletion was significant mathematically (more than 5% of TBK lost) in 7 patients, but not significant physiologically (less than 15% of TBK lost) in any except in one, who may have had other reason for TBK depletion. Although propranolol prevented the increase in PRA and aldosterone excretion, it did not prevent the modest TBK depletion. Dietary potassium intake may have some importance in the maintenance of normal body potassium during chronic treatment with thiazides for hypertension.
Hyperchloremic acidosis during the recovery phase of diabetic ketosis.
We have studied 35 patients to find the occurrence of hyperchloremic acidosis during the recovery phase of diabetic ketoacidosis. At admission the patients had typical normochloremic acidosis, with increased anion gap exactly balancing decreased serum bicarbonate. In contrast, in 18 patients with phenformin-induced lactic acidosis, the increase in anion gap at admission was much greater than the decrease in bicarbonate. The difference between lactic acidosis and ketoacidosis may be explained by a slower rate of excretion of lactate than of ketone anions. After the patients with ketoacidosis were treated, the acidosis became predominantly hyperchloremic with normal anion gap. Failure to normalize serum bicarbonate is attributed to excretion of ketone anions in the urine.
Energy production and utilization by human platelets in the presence of some guanidines and phenols (uremic toxins) that inhibit aggregation.
Platelet aggregation induced by ADP can be inhibited by plasma from uremic patients or by toxins isolated from their plasma, e.g. guanidinosuccinic acid, methylguanidine, phenol and hydroxyphenylacetic acids. Since these chemical substances can interfere with energy metabolism in tissues other than platelets and since ATP production is needed for ADP-induced aggregation, alterations in platelet energy metabolism could underlie excessive bleeding in uremic patients. Platelets incubated with idioacetate and deprived of anaerobic glycolysis produced the same quantity of ATP through respiration in the presence of all the uremic toxins studied as in their absence. Similarly, platelets incubated with cyanide and deprived of the oxidative pathway utilized anaerobic glycolysis to produce normal quantities of ATP in the presence of all the uremic toxins. The utilization of ATP, as indicated by active transmembrane potassium transport, was also unaffected by the above listed guanidines and phenols. It is concluded that the in vitro inhibition of ADP-induced platelet aggregation by the guanidines and phenols studied is not due to inhibition of production or utilization of ATP.
An osmometric method for measurement of total CO2.
Explore the source record for details and available documents.
Content and distribution of water and electrolytes in maitenance hemodialysis.
A group of patients whose dietary potassium was unrestricted and who received 12-18 h of Kiil dialysis twice weekly against a bath containing no potassium, had body potassium concentrations (total body potassium/intracellular volume) of 7.6% lower than normal. Despite marked hypokalemia at the end of dialysis, suprisingly few electrocardiographic changes were seen. Another group of subjects, dialyzed fro 5-6 h thrice weekly against a bath containing 1 mEq/liter of potassium in a Dow dialyzer, showed more marked electrocardiographic abnormalities despite smaller alterations in transmembrane potassium gradients. Rapidity of establishment of potassium gradients is important as well as magnitude. The following changes occur in a single dialysis: 100 mEq of cell potassium and 20 mEq of extracellular potassium leave the body; 100 mEq of extracellular sodium enter the cells and 415 mEq of extracellular sodium leave the body; 3.5 liters of water leave the extracellular fluid, 2.5 liters into the bath and 1 liter into the cells.
Treatment of hypertension with a combination of prazosin and polythiazide.
Preliminary results of a study of 20 patients show a combination of prazosin and polythiazide to be effective in controlling hypertension not responsive to the diuretic alone. The maximum useful dosage of prazosin was not defined, but increasing the dosage above 15 mg a day did not improve control of blood pressure.
The development of an active transport system for potassium in the embryonic avian erythrocyte.
Explore the source record for details and available documents.
A mechanism for hyporeninemic hypoaldosteronism in chronic renal disease.
Explore the source record for details and available documents.