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Biomedical subjects

J A Parsons

Publications and source records attributed to J A Parsons.

At least 145 records · Page 8Linked to original sources
PubMed1971

Cat assay for the emetic action of digitalis and related glycosides (digitoxin, digoxin, lanatoside C, ouabain and calactin).

1. A titration assay with two end points is described for comparison of the emetic and lethal potencies of digitalis-like drugs.2. A drug was infused at constant rate to a conscious, unrestrained cat, through an indwelling venous cannula. At the moment of vomiting the cat was rapidly anaesthetized and infusion continued at the same rate until the moment of cardiac arrest.3. With very slow and very fast infusions, the emetic and lethal doses tended to rise. In the range between these extremes (which varied from drug to drug) they were independent of time.4. The observations could be accounted for by analogue computation, assuming that the drugs entered an initial pool and were distributed at finite rates to receptors in the CNS (vomiting centre) and heart.5. Half times of metabolic loss derived from this computation for digitoxin, digoxin and ouabain (17, 9.9 and 1.8 h, respectively) were in the same ratio as the threefold longer half times reported for these drugs in man.6. When measured with infusion rates in the time independent range, the ratio of lethal to emetic doses did not vary between the drugs studied. All caused vomiting at 40% of the lethal dose.7. From a review of the literature, the emetic and cardiotoxic actions of digitalis-like drugs appear inseparable and probably share a common biochemical mechanism.8. It is concluded that foreseeable improvements in digitalis-like drugs are small and would depend on the elimination of any local emetic effect on gut receptors which they may have.

Animals↗
PubMed1970

Effects of cations on prolactin and growth hormone secretion by rat adenohypophyses in vitro.

1. Explants of rat adenohypophyses were incubated in medium 199, Earle's saline, or modified Earle's saline (K-Earle's) with different calcium, magnesium, sodium and potassium concentrations for 4-6 hr at 37 degrees C in 5% CO(2) in O(2).2. The amount of prolactin and growth hormone in explants and in medium was estimated by disk electrophoresis and densitometry.3. Low calcium inhibited prolactin secretion by 40-60%. Low magnesium and slightly increased (5x) magnesium (4.1 mM) did not influence prolactin secretion in either 1.8 mM or low calcium, but 10 and 20 mM magnesium inhibited secretion by 50 and 70%, respectively. Inhibition of prolactin secretion by high magnesium was reversible.4. Decreasing sodium by 80% had no effect on prolactin secretion, but low sodium inhibited the sustained, although not acute, secretion of this hormone.5. Low potassium did not affect the secretion of either prolactin or growth hormone. Increased potassium (32 or 54 mM) slightly stimulated prolactin secretion by adenohypophyses of males but had no effect on the secretion of this hormone by female glands.6. In 1.8 mM calcium, growth hormone secretion by pituitaries of males and females was markedly stimulated by increased potassium, but it was not appreciably affected by high potasium in low calcium. Increased potassium did not stimulate growth hormone secretion in medium containing low sodium with normal calcium.7. Secretion of prolactin and growth hormone by rat adenohypophyses is dependent upon calcium, but only growth hormone secretion is markedly stimulated by increased potassium. The difference in responsiveness to increased potassium, between the somatotrophs and lactotrophs, may be related to the predominant mode of hypothalamic control of these hormones.

Animals↗