POTENTIATION OF THE VASOCONSTRICTOR ACTION OF TOPICAL NOREPINEPHRINE ON THE HUMAN BULBAR CONJUNCTIVAL VESSELS AFTER TOPICAL APPLICATION OF CERTAIN ADRENOCORTICAL HORMONES

Abstract

Studies were undertaken to estimate whether adrenocortical steroids can directly potentiate the vasoconstrictor activity of norepinephrine in the intact human being and whether this property is shared equally by various adrenal steroids. Most of the 21 subjects were in good health; 5 had migraine. Under direct visualization with a slit-lamp microscope the bulbar conjunctival capillary beds were inspected for basal activity and measurement of the thresholds for vasoconstriction following topically administered serial dilutions of norepinephrine. A 2.5 per cent ophthalmic suspension of either cortisone, hydrocortisone, [DELTA] 1-cortisone, compound A, compound S or DCA was then instilled into one eye and basal activity and norepinephrine thresholds estimated again fifteen minutes later. The other eye served as control. It was demonstrated that hydrocortisone and cortisone consistently induced a threefold increase in sensitivity to norepinephrine, and [DELTA] 1-cortisone induced a tenfold increase. Compounds A and S, on the other hand, had no effect. DCA was active in 4 of 10 subjects, causing a seventeenfold increase in sensitivity, on the average; in 6 subjects, however, it had no effect. No alteration in thresholds was noted in the control eye, indicating a direct action of the steroid on the blood vessels. Only [DELTA] 1-cortisone and DCA, when active, produced a change in the basal morphology of the vessels. It is concluded that certain adrenocortical steroids can potentiate the vasoconstrictor action of norepinephrine, and that this activity does not appear to parallel the carbohydrate-regulating or salt-retaining effects of the steroid, but exists as an independent process.