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P Ogden

Publications and source records attributed to P Ogden.

16 recordsLinked to original sources
PubMed2000

Telephone medicine for internists.

The role of the telephone in medical practice is important, but often problematic. Mistakes in telephone diagnosis and triage can have severe consequences. An effective office system can reduce liability risks, and in some cases telephone contact can substitute for office visits. Internists feel unprepared to provide telephone care. Therefore, residency education needs to focus on documentation, consultant availability, and performance feedback. Research should focus on improving outcomes, reimbursement issues, and technologic advances. This article describes internists' telephone interactions with ambulatory patients, preparation for telephone medicine, and aspects of office telephone systems and makes comparisons with other primary care fields.

Ambulatory Care↗
PubMed1986

Effect of serum on sodium pump activity at various concentrations of internal and external sodium in mouse (3T3) and human (HeLa) cells.

Serum causes a large rise in the ouabain-sensitive K influx in 3T3 and other cells. It has been argued that this is secondary to the increased Na and K leaks which are also caused by serum. We have measured the K influx into 3T3 and HeLa cells at various values of intracellular Na concentration ([Na]i), and from Na-free medium in 1 and 20% (v/v) serum. Raising [Na]i increases the K influx, but saturation does not occur over the range of [Na]i studied. The estimated Km for [Na]i is around 130 mM and the Vmax some 10 times that of the resting K influx at normal (20 mM) [Na]i. Serum stimulates the K influx by a constant proportion at all values of [Na]i studied, and in Na-free medium. These results are inconsistent with previous explanations of the serum stimulation of pumping.

Animals↗
PubMed1983

The effects of chloroquine and other weak bases on the accumulation and efflux of digoxin and ouabain in HeLa cells.

We have studied the effects of the weak bases chloroquine, NH4Cl and amantadine on the handling of certain cardiac glycosides by HeLa cells. When these weak bases are applied acutely to HeLa cells they have only minor effects on the binding of cardiac glycosides to the sodium pumps and on the recovery of pump function following block. When cells are grown in these weak bases there is a variable (10-30%) reduction in pump numbers. This effect is additive to that of chronic treatment with cardiac glycosides. If all sodium pumps are blocked with ouabain, digoxin or digitoxin then recovery of function recovers with a T1/2 of about 7 h (10% h-1); digoxin and digitoxin molecules are excreted at a similar rate but ouabain excretion occurs at a much slower rate (3% h-1). These weak bases greatly slow (x 3) the rate of excretion of digoxin and digitoxin but do not alter that of ouabain. The process affected by chloroquine was estimated to have a T1/2 of 8 h. Cells grown in the presence of cardiac glycosides accumulate large numbers of glycoside molecules; chloroquine, NH4Cl and amantadine increase the accumulation of digoxin and digitoxin and may decrease that of ouabain. Quantitatively these results fit a model whereby cardiac glycosides are accumulated by HeLa cells bound to the sodium pumps, are processed by the lysosomes and then excreted. The results are consistent with a process of internalisation and renewal of sodium pumps by HeLa cells.

Amantadine↗
PubMed1982

Effects of ouabain and osmolarity on bumetanide-sensitive potassium transport in simian virus-transformed 3T3 cells.

Unidirectional potassium influx in simian virus-transformed 3T3 cells was dissected into a ouabain-inhibitable "pump' component, a bumetanide-sensitive and chloride-dependent "cotransport' component, and a residual "leak' flux. The bumetanide-sensitive component was stimulated 2-3-fold by a 60-min preincubation with ouabain. Subsequent washing of the cells and incubation in ouabain-free saline reversed both the inhibition of the Na+ pump and the stimulation of bumetanide-sensitive flux. Bumetanide-sensitive potassium influx was also stimulated by hypertonic cell shrinkage (induced by 0.1 M or 0.2 M sorbitol). This latter observation suggests that the bumetanide-sensitive system may play a role in cellular volume regulation.

Animals↗
PubMed1982

K+ transport in "tight' epithelial monolayers of MDCK cells.

Bidirectional transepithelial K+ flux measurements across 'high-resistance' epithelial monolayers of MDCK cells grown upon millipore filters show no significant net K+ flux. Measurements of influx and efflux across the basal-lateral and apical cell membranes demonstrate that the apical membranes are effectively impermeable to K+. K+ influx across the basal-lateral cell membranes consists of an ouabain-sensitive component, an ouabain-insensitive component, an ouabain-insensitive but furosemide-sensitive component, and an ouabain- and furosemide-insensitive component. The action of furosemide upon K+ influx is independent of (Na+ - K+)-pump inhibition. The furosemide-sensitive component is markedly dependent upon the medium K+, Na+ and Cl- content. Acetate and nitrate are ineffective substitutes for Cl-, whereas Br- is partially effective. Partial Cl- replacement by NO3 gives a roughly linear increase in the furosemide-sensitive component. Na+ replacement by choline abolishes the furosemide-sensitive component, whereas Li+ is a partially effective replacement. Partial Na+ replacement by choline abolishes the furosemide-sensitive component, whereas Li+ is a partially effective replacement. Partial Na+ replacement with choline gives an apparent affinity of approximately 7 mM Na, whereas variation of the external K+ content gives an affinity of the furosemide-sensitive component of 1.0 mM. Furosemide inhibition is of high affinity (K1/2 = 3 micrometer). Piretanide, ethacrynic acid, and phloretin inhibit the same component of passive K+ influx as furosemide; amiloride, 4,-aminopyridine, and 2,4,6-triaminopyrimidine partially so. SITS was ineffective. Externally applied furosemide and Cl- replacement by NO3- inhibit K+ efflux across the basal-lateral membranes indicating that the furosemide-sensitive component consists primarily of K:K exchange.

Animals↗
PubMed1981

Occurrence of passive furosemide-sensitive transmembrane potassium transport in cultured cells.

Furosemide (1 x 10(-4) M) inhibits a proportion of the total passive (ouabain-insensitive) K+ influx into primary chick heart cell cultures (85%), BC3H1 cells (75%), MDCK cells (40%) and HeLa cells (57%). This action of furosemide upon K+ influx is independent of (Na+ + K+)-pump inhibition since the furosemide-sensitive component of the K+ influx is identical in the presence and absence of ouabain (1 x 10(-3) M). For HeLa cells the passive, furosemide-sensitive component of K+ influx is markedly dependent upon the external K+, Na+ and Cl- content. Acetate, iodide and nitrate are ineffective as substitutes for Cl-, whereas Br- is partially effective. Partial Cl- replacement by NO3- gave an apparent affinity of 100 mM [Cl]. Na+ replacement by choline+ abolishes the furosemide-sensitive component, whereas Li+ replacement reduces this component by 48%. Partial Na+ replacement by choline+ gives an apparent affinity of 25 mM [Na+]. Variation in the external K+ content gives an affinity for the furosemide-sensitive component of approx. 1.0 mM. Furosemide inhibition of the passive K+ influx is of high affinity, half-maximal inhibition being observed at 5 x 10(-6) M furosemide. Piretanide (1 x 10(-4) M) and phloretin (1 x 10(-4) M) inhibit the same component of passive K+ influx as furosemide; ethacrynic acid and amiloride (both 1 x 10(-4) M) partially so. The stilbene, SITS (1 x 10(-6) M), was ineffective as an inhibitor for the furosemide-sensitive component.

Animals↗
PubMed1981

Autoradiographic localisation of [3H]ouabain bound to cultured epithelial cell monolayers of MDCK cells.

[3H]Ouabain binding to intact MDCK (cultured monolayers of dog kidney) cells of 60 serial passages is dependent upon ouabain concentration, time and medium K+. By utilising high K+ incubations to estimate non-specific [3H]ouabain-binding, the concentration of ouabain giving half maximal specific binding was estimated to be 1.0 . 10(-7) M and the total maximum binding to be 2.33 . 10(5) sites/cell. Ouabain inhibition of (Na+, K+)-pump function was monitored by the cellular uptake of 86Rb over 5 min. The larger fraction of 86Rb uptake was ouabain sensitive and the ouabain concentration giving half-maximal inhibition was 2 . 10(-7) M. The cellular distribution of the (Na+ + K+)-ATPase was investigated using [3H]ouabain autoradiography of intact freeze-dried epithelial monolayers of MDCK cells grown upon millipore filter supports. Binding of [3H]ouabain is localised over the lateral cellular membranes. Autoradiographic silver grain density is close to background levels over both the apical and basal (attachment) membranes.

Animals↗
PubMed1981

Down-regulation of the sodium pump following chronic exposure of HeLa cells and chick embryo heart cells to ouabain.

1 HeLa cells and primary cultures of embryonic chick heart cells were grown in medium containing low concentrations of ouabain for 24 h. 2 Compared with normal cells, cells grown in ouabain have fewer free sodium pump sites, an increased intracellular sodium concentration and a decreased intracellular potassium concentration. The cells are able to maintain their intracellular ion contents because the remaining pump sites have an increased turnover rate. 3 When cells that have been chronically exposed to ouabain are returned to normal growth medium, the sodium pump site numbers increase; the recovery process begins within 6 to 8 h and is complete within 24 h. Recovery of pump site numbers is primarily dependent upon de novo protein synthesis since the protein synthesis inhibitor, cycloheximide, prevents recovery.

Animals↗