ABSTRACT
Light onset or drinking alcohol causes the standing potential of the eye to rise and then fall to a trough (the EOG). After allowing for the time for the alcohol to be absorbed into the blood stream, the changes of current with time are identical for the two agents but each acts through a separate pathway, on the same effector mechanism. We have shown that +ve and -ve processes of the alcohol-EOG may be differentially affected in disease. We have now determined the separate dose-response relationship of the two voltage changes. Alcohol diluted with water was given by mouth to fasting dark-adapted subjects. Recordings continued until both the positive peak and the later negative trough were well-characterised. Doses of alcohol ranged from 3.54 to 450 mg Kg(-1) of body weight. Experiments were carried out on three normal subjects, 4-8th decade. The results are consistent with the hypothesis that each voltage change is determined by the relation: [EtOH] x [R] <--> [EtOH.R], where <--> represents a reversible reaction. For the +ve peak, semi-saturation occurs at approximately 35 mg Kg(-l). For the -ve trough it is smaller, 11 mg Kg(-l). Therefore the result is consistent with there being 2 distinct processes, and the human EOG cannot be a single 'damped oscillation'. During the short period when change of blood alcohol concentration is effective in causing the EOG sequence (using doses which provoke large voltage changes), the computed blood concentration varies from 0.01 to 0.1 mM, i.e. is > 2 orders of magnitude less than the levels required for intoxication.
Subject(s)
Central Nervous System Depressants/administration & dosage , Electrooculography/drug effects , Ethanol/administration & dosage , Pigment Epithelium of Eye/physiology , Administration, Oral , Adult , Aged , Aged, 80 and over , Dark Adaptation , Dose-Response Relationship, Drug , Female , Humans , Male , Membrane Potentials/drug effects , Middle Aged , Pigment Epithelium of Eye/drug effects , Reference ValuesABSTRACT
PURPOSE: Alcohol (EtOH) affects the electro-oculogram (EOG) in ways very similar to light, although the two agents act on the RPE through different routes. Are the EOGs to light and to alcohol affected similarly in age-related macular degeneration (AMD) and age-related maculopathy (ARM)? METHODS: Standard eye movements and recording of EOGs were used. After 26 minutes of baseline recording in darkness, subjects were either exposed to 30 cd/m(2) light or drank 226 mg/kg alcohol (7.1% vol/vol) in water. RESULTS: In 17 patients with ARM and AMD (aged 67-86 years; mean, 77), the light-EOG was slowed in comparison to normal, and the voltage changes were somewhat reduced. The mean reduction in the alcohol-EOG (EtOH-EOG) was much greater. The reduction was equal in the two eyes, regardless of uniocular foveal impairment. Some EtOH-EOG loss occurred in patients with minor fundus changes and no loss of acuity, but the loss was greater in patients with "wet" or "dry" ARM and AMD. Grading of RPE changes correlated with the decrease in EtOH-EOG responsiveness, but not with light-EOG responsiveness. CONCLUSIONS: EtOH- and light-EOGs are affected differentially. In ARM, even with minor fundus changes, patients appear to have a general abnormality in the RPE. The alcohol response abnormality is correlated to the fundus appearance, but not with age. These results provide further evidence that EtOH acts by a pathway different from that governing the action of light. These results support histologic and other evidence that in ARM there is a functional barrier between the choroid and the RPE-retina.
