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Biomedical subjects

R H Sterns

Publications and source records attributed to R H Sterns.

47 records · Page 3Linked to original sources
PubMed1983

Abnormal norepinephrine release in uremia.

Sympathetic nervous activity, which we defined as the relative rate of appearance of norepinephrine (NE) in plasma, was investigated in normal men (control) and uremic patients with two-step steady-state cold NE infusions. Both basal venous NE and the NE metabolic clearance rate (CNE, calculated from the infusion rate and the steady-state increment in venous NE) were higher in patients than in controls. The calculated appearance rate of NE in venous plasma (CNE X basal NE) was much higher in the patients, suggesting increased NE release and therefore sympathetic nervous hyperactivity in these patients. Of interest was the fall in both CNE and NE appearance rate at the higher infusion rate in controls, but not patients. These data suggest that circulating NE may normally suppress sympathetic nervous activity, but that this negative feedback mechanism is impaired in uremia.

Adult↗
PubMed1982

Oscillations of plasma K+ and insulin during K+ infusion in awake anephric dogs.

Changes in plasma potassium ([K+]p) and insulin levels were monitored during K+ infusion in awake and anesthetized nephrectomized, splenectomized dogs. In dogs studied while anesthetized with pentobarbital, the increase in [K+]p was linear, reflecting a nearly constant rate of cellular uptake of the infused K+. In contrast, in dogs studied 18 h after nephrectomy while awake, [K+]p oscillated during infusion, reflecting an inconstant rate of cellular K+ uptake. Although these oscillations in [K+]p were associated with parallel oscillations in plasma insulin levels (suggesting the possibility of a physiological feedback control loop involving K+ and insulin), when the oscillations in insulin levels were blunted by somatostatin infusion or abolished by pancreatectomy plus insulin replacement, oscillations in [K+]p persisted and the average rate of cellular K+ uptake was not diminished. The observed oscillations of [K+]p during K+ infusion suggest the possibility of regulatory control of cellular K+ uptake within the pathophysiologic range of [K+]p. The putative control system is independent of and quantitatively more important than K+-induced insulin secretion and is obscured by pentobarbital anesthesia.

Animals↗
PubMed1981

The disposition of intravenous potassium in normal man: the role of insulin.

1. Potassium infusion causes an increase in immunoreactive insulin levels in dogs, but either a small (30%) or no increase in humans. Since insulin stimulates the uptake of K+ by cells, a regulatory role for K+-induced insulin release has been postulated. To study the role of insulin in regulating cellular K+ uptake, six fasting normal volunteer subjects underwent two K+ infusions on separate days. Both infusions delivered 0.6 mmol h-1 kg-1 for 3 h. In one subject glucose was simultaneously infused at 0.67 mmol h-1 kg-1 (a rate known to increase peripheral insulin levels by 40-100%); the other infusion contained no glucose. 2. Plasma insulin levels did not increase during the glucose-free infusions. During glucose-containing infusions, insulin levels were 40% higher than those during glucose-free infusions. Despite this, neither urinary potassium excretion nor the increment in plasma K+ concentration or the calculated cellular K+ uptake differed significantly during the 3 h of glucose-free and glucose-containing infusions respectively. 3. These data do not support the view that potassium-induced insulin secretion regulates cellular potassium uptake within the physiological range of plasma K+ concentration.

Blood Glucose↗
PubMed1981

Internal potassium balance and the control of the plasma potassium concentration.

The plasma potassium concentration is determined both by external potassium balance and by the distribution of potassium between extracellular and intracellular fluid compartments, i.e., "internal potassium balance." Whenever external potassium balance is altered, the resultant change in the plasma potassium concentration is strongly influenced by concomitant alterations in internal potassium balance. Several factors alter internal potassium balance independently of changes in external balance. Acid-base disturbances produce shifts of potassium into or out of cells, but attempts to quantify these effects are not likely to be clinically useful. Hypertonicity produces a shift of potassium out of cells. Several hormones (insulin, aldosterone, catecholamines, glucagon, and growth hormone) may have roles in internal potassium balance. Digitalis and succinylcholine, by producing efflux of potassium from cells, may cause hyperkalemia. Potassium is released from skeletal muscle during exercise, causing an increase in the plasma potassium concentration. The periodic paralyses are associated with well-defined transient alterations in internal potassium balance.

Acid-Base Imbalance↗
PubMed1981

Effect of potassium removal during hemodialysis on the plasma potassium concentration.

The effect of potassium removal by hemodialysis on the plasma potassium concentration (PK) was observed during 20 studies on 7 anuric patients. The following was observed: (1) The pattern of change in PK is consistent with at least a two-compartment distribution; hence, in contrast to urea, PK shows a marked postdialytic rebound and the simple equation for solute removal from a single pool cannot predict postdialysis PK. (2) The magnitude of the fall in PK correlated with the predialysis PK; this was not only due to increased potassium removal, but also due to a dependence of the apparent volume of distribution of potassium on the state of potassium balance. The fractional decrement in plasma potassium concentration, contrary to that of urea, is a function of predialysis concentration, and prediction of the effect of dialysis on plasma potassium concentration can assume neither a single pool nor a constant distribution volume for this ion.

Blood Urea Nitrogen↗
PubMed1979

Disposition of intravenous potassium in anuric man: a kinetic analysis.

The disposition of a constant-rate (0.3 mEq/kg/hr) intravenous potassium load was studied in anuric, chronic hemodialysis patients. Changes in plasma potassium concentration could be adequately described by a two-compartment kinetic model under both isohydric conditions and during acute metabolic alkalosis. From 63 to 92% of the infused potassium left the extracellular fluid (ECF) in isohydric studies, and from 73 to 97% left the ECF in alkalanizing studies. Cellular uptake of the infused potassium was less when the plasma potassium concentration was higher. Plasma aldosterone levels rose but insulin levels did not increase during infusions. In a juvenile-onset diabetic subject, the impairment of cellular potassium uptake at higher plasma potassium was magnified so that infused potassium was virtually confined to the ECF compartment until exogenous insulin was given. This implies a permissive rather than a regulatory role for endogenous insulin in facilitating cellular entry of excess potassium.

Anuria↗