Impaired vision in the elderly: a preventable condition.

BACKGROUND: Vision is thought to deteriorate with age as a number of factors in later life endanger eyesight. Assessment of the visual acuity of the elderly and identification of endangering factors help in detecting those with impaired vision which in turn impairs daily activities. OBJECTIVE: This study measured the visual acuity of the senior citizens and identified those with impaired vision. The probable contributing factors for impaired vision were studied with the aim of preventing visual impairment. METHOD: The study was part of a screening campaign for elderly glaucoma in the community. A convenience sample of ambulatory senior citizens from stratified localities had their visual acuity measured with a standard Snellen's chart. The test was repeated with pinholes if the visual acuity was less than 0.5. Those without improvement after pinhole were considered as having impaired vision. People with elevated intraocular pressure by the Pulsair were selected for examination by an ophthalmologist for ocular pathology. RESULTS: For the ambulatory population aged > or = 65 the mean visual acuity of either eye before pinhole was 0.3. Nearly 72% had impaired vision (visual acuity not corrected above 0.5 with pinhole). There was a significant association between this impairment and female sex, history of diabetes mellitus or glaucoma, cataract, and infrequent eye examination. CONCLUSION: Impaired vision is highly prevalent in the elderly ambulatory population, a condition which is preventable by tight surveillance of predisposing factors and regular simple measurement of visual acuity. The primary care setting is most suitable for these activities.

Inability of indomethacin to modify hydrochlorothiazide diuresis and natriuresis by the chimpanzee kidney.

A drug interaction study in the chimpanzee by using indomethacin and hydrochlorothiazide has shown conclusively that the diuretic and saluretic properties of hydrochlorothiazide were not compromised by indomethacin. This was true whether hydrochlorothiazide or indomethacin was administered first. The renal clearance of hydrochlorothiazide was not influenced by indomethacin nor was the renal clearance of indomethacin significantly altered by hydrochlorothiazide. Indomethacin alone caused a small but significant increase in sodium, potassium and chloride excretion and in Curate/glomerular filtration rate. In control experiments with placebo, potassium excretion was also significantly increased. The implications of these observations remain obscure. In all experiments utilizing hydrochlorothiazide, the well known renal effects of this agent were clearly evident under these experimental conditions.

Does intracellular sodium regulate sodium transport across the mucosal surface of frog skin?

A method has been devised to functionally remove the serosal membrane of frog skin. Skins treated in this way have no spontaneous potential. However, if sodium gradients are placed across the tissues diffusion potentials and hence short-circuit currents of either sign, depending on the direction of the gradient, could be recorded. These short-circuit currents were completely imhibited by amiloride only from the mucosal face. However, the concentration of amiloride causing 50% inhibition of the short-circuit curent (Km) in treated skins was 2.3 . 10(-3)M, when a sodium gradient was applied from serosa to mucosa, whereas both in untreated skins without a sodium gradient and in treated skins with a mucosal to serosal sodium gradient, the Km of amiloride was 2 . 10(-7)-4 . 10(-7)M. The mechanism by which amiloride is able to inhibit the short-circuit currents of either sign is discussed.

Interdependence of the two borders in a sodium transporting epithelium. Possible regulation by the transport pool.

Specific binding of 14C-amiloride to the mucosal surface of frog skin epithelium (Rana temporaria) has been used as a measure of the number of sodium entry sites. All binding measurements were made with the mucosal surface bathed in a solution containing 1.1 mM sodium. When manipulations were used which increased the intracellular concentration of sodium the amount of amiloride bound was reduced. The manipulations included flushing the mucosal surface with solutions containing 111 mM sodium after serosal efflux was inhibited with ouabain or potassium removal. Similar results were obtained when cells were loaded with lithium. These effects on amiloride binding did not appear to depend on changes in membrane potential or upon changes in affinity of amiloride for its binding site. It appears that inhibition of serosal sodium efflux from the epithelium causes a reduction of mucosal sodium influx by making entry sites unavailable. This latter may be a result, directly or indirectly, of the sodium concentration in the sodium transport pool.

Induction of transporting sites in a sodium transporting epithelium.

1. Frogs (Rana temporaria) were bathed for 1 week in solutions containing 1-1 mM sodium chloride and either one or both of amiloride (10(-4)M) and spironolactone (10(-5r both of amiloride (10(-4) M) and spironolactone (10(-5) M). This procedure was designed to deplete the sodium transporting compartment of the skin epithelium of sodium, while at the same time antagonizing the effects of endogenous aldosterone. 2. After 1 week the skins were used in vitro to measure the level of sodium transport (short-circuit current) and the density of sodium entry sites in the mucosal surface of the epithelium ([14C]amiloride binding). 3. Sodium deprivation for 1 week caused approximately a doubling of both sodium transport and the density of sodium entry sites in the mucosal surface of the epithelium compared to control skins. 4. When the results for sodium deprived and control skins were pooled there was a highly significant correlation between the density of sodium entry sites and sodium transport. 5. Mechanisms by which sodium deprivation leads to an increase in the density of sodium entry sites are discussed.

Estimation of the lifespan of amiloride binding sites in the membranes of toad bladder epithelial cells.

1. Sodium entry sites in the membranes of isolated epithelial cells prepared from bladders of toads (Bufo marinus) have been labelled with amiloride. The number of binding sites remained constant in suspensions for up to 100 hr. 2. In the presence of a protein synthesis inhibitor (cycloheximide, 0-5 mug/ml.) there was a decline in the density of binding sites was approximately exponential. Regression analysis gave a half-life of approximately 60 hr. 3. Aldosterone (5 X 10(-8) M) caused a significant (P less than 0-001) increase (50%) in the density of amiloride binding sites. Cells which had been treated with aldosterone had populations of binding sites which declined, in the presence of cycloheximide, at rates indistinguishable from those of untreated cells.

Characteristics of the entry process for sodium in transporting epithelia as revealed with amiloride.

1. The permeation of sodium ions trhough the mucosal surface of frog skin epithelium at different transepithelial potentials has been investigated using the blocking drug amiloride. 2. An increase in serosal negativity in voltage-clamped skins was associated with an increase in the absolute amount of inhibition caused by a fixed concentration of amiloride. Hyperpolarizing or depolarizing skins with respect to the short-circuited condition did not affect the apparent affinity of amiloride for the entry sites. 3. When skins were voltage clamped at -50 mV (serosa negative) the specific binding of amiloride to sodium entry sites was increased by 77% compared to the short-circuited condition. Skins clamped at +50 mV had only 72% of the specific binding found in short-circuited skins. Experiments with a second blocking drug, triamterene, indicated that the extra binding sites appearing at -50mV were similar to those found under short-circuit conditions. The appearance and disappearance of binding sites may reflect changes in cell volume. 4. The findings suggest that the increased sodium current which flows when skins are clamped at -50 mV results from an increase in the number of entry sites, and perhaps also to a voltage sensitive increase in flux through each entry site.