ABSTRACT
Isolated corneas were mounted in Ussing-Zerahn-type chambers and short circuit current (SCC) was measured before and after application of drugs (5 X 10(-5) mol X 1(-1)) interfering with adrenergic receptors. Epinephrine increased SCC in the rabbit cornea and decreased SCC in the human cornea. alpha-Adrenergic stimulation or inhibition did not affect SCC. The increase in SCC observed after terbutaline (beta 2-agonist) was similar to the increase after isoproterenol (beta 1- and beta 2-agonist). SCC was not influenced by the beta 1-antagonist atenolol but was modified, although differently in rabbit and man, by the beta 1- and beta 2-antagonist propranolol. Thus, the catecholamine response of the rabbit and human cornea is mainly mediated by beta 2-adrenergic receptors. However, species differences were observed when testing the effect of propranolol on the transcorneal flux of 22Na and 36Cl. In the rabbit cornea the net Cl flux (directed from the aqueous to the tear side) was inhibited by propranolol, whereas net Na flux (from the tear to the aqueous side) was not influenced by the drug. In the human cornea propranolol reduced unidirectional Na flux from the aqueous to the tear side. Thus, the regulatory effect of propranolol on corneal transparency is different in man and the rabbit.
Subject(s)
Chlorides/metabolism , Cornea/metabolism , Ion Channels/metabolism , Receptors, Adrenergic, beta/metabolism , Sodium/metabolism , Adrenergic beta-Agonists/pharmacology , Adrenergic beta-Antagonists/pharmacology , Animals , Cornea/drug effects , Dose-Response Relationship, Drug , Humans , In Vitro Techniques , Ion Channels/drug effects , Rabbits , Receptors, Adrenergic, beta/drug effectsABSTRACT
The pH value in human precorneal tear film was measured with micro- and semimicro-pH-electrodes; the mean was pH 7.6. Stimulation of tear secretion and blinking led to a decrease in the pH value. When the eyelid was open, the precorneal tear film was alkalized by equilibration with the partial pressure of the CO2 in the surrounding air. When the eyelid remained open for 60 s or longer, an equilibrium value of greater than pH 9 was attained.
Subject(s)
Microelectrodes , Tears/physiology , Blinking , Humans , Hydrogen-Ion Concentration , Tears/metabolismABSTRACT
Sodium and chloride net transport in isolated human cornea preparations were found to be pH dependent. Sodium net transport was directed from aqueous humor to tear side at pH 7.6 and 8.6. At pH 7.4, net sodium flux did not differ significantly from zero, and at pH 7.0, net sodium transport was directed toward the aqueous humor side. Chloride net flux at pH 8.6 and 7.6 was also directed from aqueous humor to tear side. Acidification of the bathing solution to pH 7.4 and 7.0 was followed by a decrease in chloride net fluxes to values not significantly different from zero.
Subject(s)
Chlorides/physiology , Cornea/physiology , Sodium/physiology , Biological Transport , Electrophysiology/instrumentation , Electrophysiology/methods , Humans , Hydrogen-Ion Concentration , In Vitro TechniquesABSTRACT
22Na and 36Cl fluxes in isolated human cornea preparations were measured under short-circuited conditions. At pH 7.3-PH 7.6 sodium net flux was directed from aqueous humour to tear side, chloride net flux was statistically not different from zero. Alkalinization of the bathing solution to pH 8.6 stimulated unidirectional sodium and chloride fluxes from aqueous humour to tear side resulting in net sodium and chloride fluxes towards the tear side which both were statistically different from zero. Cyclic AMP (10(-3) M) was found to stimulate sodium and chloride unidirectional fluxes from aqueous humour to tear side, thus leading to significant net sodium and chloride fluxes in the same direction. Epinephrine (10(-4) M) increased the unidirectional chloride flux from aqueous humour to tear side more pronounced than in the opposite direction, producing a significant net chloride flux towards the tear side. The results are consistent with the hypothesis that the electrolyte pumps may under certain conditions contribute to the dehydration of the stroma.
