The blood spot thyrotropin method is not adequate to screen for hypothyroidism in the elderly living in abundant-iodine intake areas: comparison to sensitive thyrotropin measurements.

We investigated whether the blood spot thyrotropin (TSH) method was adequate for screening elderly subjects with abundant iodine intake (median excretion 330 microg/g creatinine) for hypothyroidism. In 97 healthy adults (group A), 210 nursing home residents (group B) and 265 elderly subjects living at home (group C) serum (sensitivity < 0.02 mU/L, cost 1.2 U.S. dollars [USD]) and blood spot TSH (sensitivity < 1.0 mU/L, cost 0.4 USD) were measured, and the sensitivity and specificity of different blood spot TSH cutoff points to detect cases with elevated serum TSH were calculated. Elevated (> 3.5 mU/L) serum TSH levels (group A, 6.2%; group B, 16.2%; group C, 22.3%; B > A, p = 0.025; C > A, p < 0.001) were detected with the required sensitivity of greater than 0.9 only if the cutoff point of the blood spot TSH was set as low as 2.5 mU/L, but this led to a considerable loss of specificity. At cutoff point 2.5 mU/L, the rate of positivity was 39.3% and the cost of blood spot screening/person increased to 0.88 USD, considering that positive cases have to be rechecked by serum TSH to exclude false positivity. Cases with significantly elevated (> 10.0 mU/L) serum TSH (group A, 1.03%; group B, 2.85%; group C, 2.20%) were detected at blood spot cutoff points 10.0-4.0 mU/L with a sensitivity of 1.0 and without considerable loss of specificity. We conclude that while screening for hypothyroidism in the elderly population with abundant iodine intake is justified by the high prevalence of elevated ultrasensitive serum TSH values, the sensitivity of the blood spot method is insufficient to detect the subclinical hypothyroidism accurately and would, therefore, fail to detect most affected subjects.

Actinomycin D suppresses the protective effect of dexamethasone in rats affected by global cerebral ischemia.

Simultaneous occlusion of both common carotid arteries in female Sprague-Dawley CFY rats produced characteristic symptoms of global cerebral ischemia, such as staggering, circling, convulsions, followed by coma and death. A close correlation existed among these symptoms and the elevation of water and Na+ content, appearing at the stage of staggering; Evans blue extravasation and diminution of K+ content, detected at circling; and the increase in Ca2+ content in the total brain tissue, manifesting itself at the phase of convulsions, indicating the development of cerebral edema due to ischemia. Dexamethasone given subcutaneously in a single 2.0 mg kg-1 dose 5 hours prior to the induction of global cerebral ischemia reduced considerably the morbidity and mortality, the alterations in water and electrolyte content, and albumin leakage in the brain tissue. Actinomycin D, in a dose of 0.5 mg kg-1 injected intravenously 1 hour before steroid treatment, abolished the beneficial effect. This finding suggests that de novo protein synthesis is involved in the cerebroprotective effect of dexamethasone.

On the late antiischaemic action of the stable PgI2 analogue: 7-oxo-PgI2-Na and its possible mode of action.

Earlier we have shown in the dog model mimicking angina on effort a delayed antiischaemic effect of PgI2 and its stable analogue 7-oxo-PgI2-Na, appearing only when the drug induced marked vasodilatation was over [1]. In the present experiments we could show that the protective effect appears at a time when the blood pressure returned to normal and in addition the marked platelet aggregation inhibitory effect has also faded away. In the rat 7-oxo-PgI2 could substantially diminish vasopressine induced T-wave elevation in the ECG if given 2 hours before administration of vasopressin. In addition it could moderate the vasopressin induced metabolic changes appearing as diminution of the myocardial CP and ATP-level and increase of the myocardial lactate content. A similar metabolic protection was found in the heart of rats pretreated with 7-oxo-PgI2 2 hours before taking myocardial samples and exposing them for 1 minute to ischaemia by incubation in Ringer solution. It is concluded that a direct metabolic and hemodynamic effect could be at least partly responsible for the late antiischaemic effect of 7-oxo-PgI2. This effect was also present in the early phase of experimental myocardial infarction in conscious rats if animals were pretreated with 7-oxo-PgI2 2 hours before occlusion. However treatment did not increase survival rate and failed to reduce the incidence and severity of arrhythmias.

Relationship between blood flow velocity in the choroid and intraocular pressure in rabbits.

By using thermistors for calorimetry to monitor blood flow velocity in the choroid of the anaesthetized rabbit, it was found that an elevation of intraocular pressure reduced the choroidal blood flow. The relationship between the ratio of perfusion pressure to intraocular tension (x) and the reciprocal value of the percentage of blood flow velocity (l/y) showed a curve convex towards the pressure axis. On a log-lin scale the graph was linear. A significant linear correlation with a coefficient of 0.965 was obtained. The regression equation was found to be log l/y = 0.48x-1.98 +/- 0.29. From the present experiments it is concluded that the vascular bed of the choroid in the rabbit is a passive one with no sign of autoregulation. The observations are discussed from the point of view of blood supply and possible damage to the optic disc.

Effect of prostaglandin E2 on the permeability of the iris vessels to horseradish peroxidase in the rabbit.

Prostaglandin E2 (0.5 microgram in 10 microliter 10% ethanol) was introduced into the anterior chambers of rabbit eyes. Using the horseradish peroxidase method, it was shown under the electron microscope that the endothelial barrier of the iris vessels broke down. The peroxidase penetrated as far as the basis of the posterior epithelial cells, however, without entering their lateral intercellular spaces. The question of whether the effect of prostaglandins on the barrier was a direct effect or at least a partially indirect one, i.e., a haemodynamic action, is discussed.

Effect of prostaglandin E2 on the isolated rabbit iris sphincter.

Experiments on twenty-eight New Zealand albino rabbits have shown that prostaglandin E2 causes contraction of the isolated iris sphincter and is about five times as effective as acetylcholine. Prostaglandin E2 does not act on the cholinergic receptors; the effect of prostaglandin E2 was not increased by eserine, and not abolished by atropine. In high doses indomethacin (3 X 10(-4) M) reversed the prostaglandin effect, but lower concentrations (3 X 10(-5) M) left it unaffected.