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Biomedical subjects

K M Nelson

Publications and source records attributed to K M Nelson.

At least 55 records · Page 3Linked to original sources
PubMed1985

Alteration of adipocyte calcium homeostasis by Escherichia coli endotoxin.

The present study evaluated calcium homeostasis in rat adipocytes after either in vivo or in vitro exposure to Escherichia coli endotoxin. Fat cells from endotoxin-treated rats showed an enhanced uptake of 45Ca. In an attempt to differentiate between 45Ca binding to the cell surface and intracellular 45Ca accumulation, adipocytes were exposed to 5 mM LaCl3. The amount of 45Ca remaining associated with lanthanum-treated adipocytes was taken to be located intracellularly and was increased in adipocytes from endotoxin-treated rats. The amount of 45Ca displaced by lanthanum was also increased in adipocytes from endotoxin-treated rats. This suggested that the endotoxin-induced increase of 45Ca accumulation included both cell surface and intracellular binding sites. Compartmental analysis of the exchange kinetics of cell-associated 45Ca with 40Ca in the medium indicated a 77% increase in the size of the cell surface compartment of adipocytes from endotoxin-treated rats compared with controls. In addition, endotoxin treatment altered the flux of calcium from the cells to the medium. In vitro exposure of freshly prepared adipocytes to 250 or 750 micrograms endotoxin/ml did not produce a perturbation of adipocyte calcium homeostasis. The results indicate that endotoxin induces alterations in the ability of adipocytes to regulate calcium translocations, suggesting that some metabolic and hormonal aspects of endotoxins' actions may be mediated through perturbation of cellular calcium homeostasis.

Adipose Tissue↗
PubMed1983

Salicylate determined with a microcentrifugal analyzer, and compared with Du Pont aca, trinder, and liquid-chromatographic methods.

We describe a new automated method for measuring serum salicylate in the Multistat III microcentrifugal analyzer. Ferric nitrate reagent and serum blanking are used. We compare this new method, the automated Du Pont aca method, and the manual Trinder method with a "high-performance" liquid-chromatographic method. The unblanked Trinder method had the poorest correlation (r = 0.980, Sy X x = 19.1) with the chromatographic method. The serum-blanked aca and Multistat III methods showed better correlation (r = 0.995, Sy X x = 9.5 mg/L, and r = 0.991, Sy X x = 13.0 mg/L, respectively) with the chromatographic method. However, we conclude that all three colorimetric methods give clinically useful results and that the increased time, expense, and expertise required for chromatographic salicylate analysis are difficult to justify in a routine clinical laboratory.

Autoanalysis↗
PubMed1981

Local effect of thermal injury on skeletal muscle blood flow and nucleotide levels.

We have previously shown that 3 days following a 3-sec scald of one hind limb, in vitro glucose utilization was markedly increased in soleus muscle from the burned limb but not in soleus from the contralateral unburned limb. The aim of the present study was to evaluate factors that might contribute to this local metabolic alteration. Three days following a 3-sec scald of one hind limb of the rat, blood flow through soleus and gastrocnemius muscles of the burned limb as measured with labeled microspheres was increased 167% (P less than 0.01) and 58% (P less than 0.04), respectively. Calf muscles of the burned limb, frozen in situ, showed a 48% decrease in ATP (P less than 0.001), 37% decrease in ADP (P less than 0.001), 192% increase in AMP (P less than 0.01), 45% decrease in total adenine nucleotides (P less than 0.001), 132% increase in pyruvate (P less than 0.001), and 377% increase in lactate (P less than 0.001). Blood flow and ATP, ADP, total nucleotides, and pyruvate levels of calf muscles of unburned limb of burned rats did not differ from controls, but AMP and lactate were increased 115% (P less than 0.05) and 144% (P less than 0.001), respectively. The decrease in ATP and increase in AMP and lactate in muscles of the burned limb suggest an increased rate of glycolysis in vivo which may be due, in part, to the stimulation of phosphofructokinase. Furthermore, the increased AMP and lactate may contribute to the increase in blood flow in muscles of the burned limb. It is proposed that thermal injury alters local adenine nucleotide levels, which results in elevated glucose utilization and blood flow in muscles of the burned region.

Adenosine Triphosphate↗
PubMed1979

Effect of traumatic injury on sensitivity to insulin.

Disturbances in carbohydrate homeostasis are metabolic hallmarks in the host response to trauma. Since alterations in insulin responsiveness, especially insulin resistance, have been related to the metabolic sequelae of shock, the present study evaluated insulin responsiveness in traumatic shock. Injury (LD50) of fasted, male Holtzman rats (115 plus or minus 20 gm) by tumbling in the Noble-Collip drum resulted in hyperglycemia in spite of a concomitant hyperinsulinemia. The ability of insulin to lower plasma glucose was evaluated at either three hours or 24 hours post-trauma by means of glucose and insulin tolerance tests. The injured rats showed glucose intolerance and hyperinsulinemia three hours after injury but showed a normal glucose tolerance and hypoinsulinemia on the day after injury. Insulin was ineffective in lowering plasma glucose at both of these times. Noble-Collip tumbling trauma induced no systemic changes in insulin responsiveness in vitro at either time as evaluated by 1) epididymal fat pad glucose oxidation of U-D-14C-glucose to 14CO2 or 2) hemidiaphragm incorporation of U-D-14C-glucose into glycogen. The data suggest that insulin resistance is not due to a decreased capacity of various tissues to respond to insulin.

Adipose Tissue↗