Hyperthermia‐induced increase in potassium transport in Chinese hamster cells

Abstract

The effect of hyperthermia (42OC) on K + transport has been examined by monitoring t h e uptake of 42KCI by Chinese hamster (line CHO) cells at both 37O and 42OC as well as 37OC following a 30-min treatment at 42OC. Early studies showed that CHO cells exhibit two components of uptake at both 37O and 42OC. Consequently, it was necessary to determine rate equations describing a three-compartment system (i.e., the bathing medium and two cellassociated compartments) and apply them to this system. Using the equations describing the behavior of the tracer in each compartment as well as the general solutions given by Robertson et al (1957), a method was developed for obtaining the two components of influx. The two transport rates were determined from equations arising from mathematical analysis and requiring only measurable quantities for their solutions. The results of this study showed that (1) both components of influx at 42OC are increased over influx at 37OC;(2) the increase is significant (by an average 68% for the rapid component and 55% for the slow component); and (3) the increase is due entirely to an increase in active transport. The increased active transport is both immediate and quickly reversible when cells are returned to 37OC; resumption of cell division is delayed for several additional hours, indicating that changes in potassium transport are not directly responsible for the prolonged delay in cell division. Rather, the results suggest that increased activity of the membrane pump may be the initial event in a series of events resulting from heat treatment.

Investigation of adenylate energy charge, phosphorylation potential, and ATP concentration in cells stressed with starvation and heat

“…In addition, heat appears to uncouple Rbf transport from ATP hydrolysis in this cell type after 40 min at 45°C (Anderson and Hahn, in press); such uncoupling would cause a major increase in ATP demand and might be involved in the heat-induced decline in cellular energy status observed in the present study. A number of other reports indicate effects of heat on ion flux and membrane potential in eucaryotic cells which might be due to ion leaks or alterations in the efficiency of active transport (Mikkelsen et al, 1981;Yi, 1979;Bowler, 1981;Stevenson et al, 1983a;and Boonstra et al, 1984). Thus, decline in energy status of heated cells due to increased energy demand for maintenance of cellular ion homeostasis may be indicated.…”

The effects of hyperthermia on mammalian cell structure and function

“…The status of ion influx and efflux after hyperthermia is equivocal. Treatment of CHO cells at 42°C led to an increase in the influx of K+ ions within 15 min, which was reversed immediately upon return to 37°C (Stevenson, Galey & Tobey 1983). A slight decrease in the total K+ content after 150 min at 42°C was seen, indicating that efflux rates also must have been changed.…”

Phrenic Nerve Injury—Yet Another Achilles' Heel for AF Ablation?

“…The former mechanism has been previously demonstrated to change resting membrane and action potential characteristics in myocardial tissue, in part due to alterations in permeability characteristics of the plasma membrane. [12][13][14][15] A possible clinical implication of these observations is that impending (irreversible) nerve injury may be averted in at least a subset of patients by carefully maintaining any evidence of phrenic nerve damage during RF ablation, for example, loss of nerve capture during high output pacing, decrease in diaphragmatic excursion, or occurrence of hiccups.…”