Nifedipine alters the light-rise of the electro-oculogram in man.

BACKGROUND: To determine if the L-type calcium channel participates in the generation of the light-rise of the electro-oculogram (EOG) in man. The aim was to use nifedipine, a specific, L-type calcium channel inhibitor and determine the effects on the light-rise of the EOG in healthy participants. METHODS: The EOG was recorded in 14 participants before and after a 10 mg oral dose of fast-acting nifedipine. The Arden index, time to peak of the EOGs and pulse were recorded before and after ingestion of nifedipine. The test-retest variability of the EOG's light-rise in the absence of nifedipine was performed on 11 of the participants. The mean ± SEM oral dose was 147 ± 9 µg/kg. Scotopic electroretinograms (ERGs) were recorded at four intensities (0.0067, 0.0849, 0.364 and 1.140 cd.s.m⁻²) in six participants before and after a 10 mg oral dose of nifedipine. RESULTS: The light-rise of the EOG was significantly reduced in five participants by -22.80 ± 5.6% (p = 0.021), whilst in four of the participants the light-rise increased by +15.7 ± 1.9% (p = 0.033). The results of the test-retest EOGs showed a range of -9.1 to +9.8% Arden index in the absence of nifedipine. Thus, the responses of five participants were not included in the analysis, as the change in the EOG with nifedipine was within this range. The differences in the time to peak of the light-rise were not significantly different in those that showed an increase (p = 0.33) or a decrease (p = 0.87) in the EOG after nifedipine. Pulse rate was not significantly different after nifedipine in the group that showed an increased light-rise (p = 0.77) or in those whose light-rise fell after nifedipine (p = 0.33). No significant effect was observed on the a- and b-wave amplitudes and implicit times for the scotopic components of the scotopic ERG. CONCLUSIONS: The L-type calcium channel contributes to the light-rise of the EOG in man.

Do mobile phone base stations affect sleep of residents? Results from an experimental double-blind sham-controlled field study.

OBJECTIVES: The aim of the present double-blind, sham-controlled, balanced randomized cross-over study was to disentangle effects of electromagnetic fields (EMF) and non-EMF effects of mobile phone base stations on objective and subjective sleep quality. METHODS: In total 397 residents aged 18-81 years (50.9% female) from 10 German sites, where no mobile phone service was available, were exposed to sham and GSM (Global System for Mobile Communications, 900 MHz and 1,800 MHz) base station signals by an experimental base station while their sleep was monitored at their homes during 12 nights. Participants were randomly exposed to real (GSM) or sham exposure for five nights each. Individual measurement of EMF exposure, questionnaires on sleep disorders, overall sleep quality, attitude towards mobile communication, and on subjective sleep quality (morning and evening protocols) as well as objective sleep data (frontal EEG and EOG recordings) were gathered. RESULTS: Analysis of the subjective and objective sleep data did not reveal any significant differences between the real and sham condition. During sham exposure nights, objective and subjective sleep efficiency, wake after sleep onset, and subjective sleep latency were significantly worse in participants with concerns about possible health risks resulting from base stations than in participants who were not concerned. CONCLUSIONS: The study did not provide any evidence for short-term physiological effects of EMF emitted by mobile phone base stations on objective and subjective sleep quality. However, the results indicate that mobile phone base stations as such (not the electromagnetic fields) may have a significant negative impact on sleep quality.

Light and alcohol evoked electro-oculograms in cystic fibrosis.

Cystic fibrosis (CF) is caused by a defect in the cystic fibrosis transmembrane conductance regulator (CFTR) which is a chloride channel. CFTR is expressed in the retinal pigment epithelium (RPE) where it is believed to be important in generating the fast oscillations (FOs) and potentially contributing to the light-electro-oculogram (EOG). The role of CFTR in the alcohol-EOG is unknown. We recruited six individuals with CF (three homozygotes for Delta508 and three heterozygous for Delta508) and recorded the light- and alcohol-EOGs as well as the FOs and compared them to a control group. The results showed that in the CF group the amplitude of the alcohol- and light-EOGs were normal. However, the time to peak of the light- and alcohol-rises were significantly faster than in the control group. We conclude that CFTR is not primarily responsible for the alcohol- or light-rises but is involved in altering the timing of these responses. The FOs showed differences between the homozygotes, heterozygotes and the controls. The amplitudes were significantly higher and the time to the dark troughs were significantly slower in the heterozygote group compared to both controls and the homozygotes. In contrast, the homozygotes did not differ in either amplitude or the timing of the FOs compared to the controls.

Alcohol- and light-induced electro-oculographic responses: variability and clinical utility.

The alcohol-induced electro-oculographic (EOG) response has been proposed by Arden as an indicator of retinal pigment epithelial (RPE) integrity. We have evaluated the consistency of the alcohol-EOG with respect to clinical applicability and compared this response to the ISCEV-standard EOG. We recorded, in a group of normal subjects (n=29, 14 men with mean age 42+/-11 years and 15 women with mean age 36+/-13 years), the alcohol response to a single oral dose of ethanol at 160 mg/kg (as 40 proof vodka, drunk in 15 s after 12 h of fasting), followed by an ISCEV-standard EOG 90 min after alcohol administration. Blood alcohol levels were monitored at regular intervals with a breath analyzer. We found a wide range of amplitudes in both light and alcohol responses among participants, from minimal to large values. Subjects had a wide range of blood alcohol concentrations from 0.02 to 0.10%; near the time of the response peak, but there was no relationship between alcohol levels and peak/baseline ratios. In addition, there was no relationship between alcohol peak/baseline ratio and the Arden ratio. Neither the alcohol nor the light response parameters showed any relationship with age or gender. Some of the inter-individual variability in the EOG response to alcohol may reflect variable absorption of oral alcohol. The alcohol-induced EOG has too broad a range of responses to be useful clinically for the one-time evaluation of individual patients. We have similar concerns regarding clinical applications of the standard light-induced EOG.

Differential effects of light and alcohol on the electro-oculographic responses of patients with age-related macular disease.

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.

The human electro-oculogram: interaction of light and alcohol.

PURPOSE: To investigate the production of the voltage changes evoked in the retinal pigment epithelium (RPE) by light and alcohol and the interaction of these agents. METHODS: The eye movement potential in humans was intermittently recorded to standard horizontal excursions for long periods during which either retinal illumination was altered or ethyl alcohol was administered by the oral, intragastric, or intravenous route. In other experiments, both light and alcohol were administered. RESULTS: Alcohol and light produced near identical corneofundal voltage changes (positive and then negative) over more than 40 minutes. Differences in timing between alcohol and light increases are explicable by the delays in alcohol absorption. Weak background light suppressed the effect of light steps, and low levels of background alcohol suppressed the response to subsequent doses. Backgrounds of one agent did not affect the voltage changes caused by the other. Minimal alcohol effects were seen after administration of 1 g orally or 270 mg intravenously--that is, doses that produced undetectable changes in breath alcohol. The semisaturating oral dose was approximately 20 mg/kg. CONCLUSIONS: Alcohol and light act through separate pathways to form a final common pathway inside the RPE cell that is responsible for triggering the timing of the slow oscillatory changes of EOG voltage. The sensitivity and duration with which alcohol affects the RPE are comparable with the effect of melatonin or dopamine, although only the former interacts with light similarly to alcohol. Transient modulation of the acetylcholine (Ach) neuronal receptor occurs at similar sensitivity, but all other known actions of alcohol require higher concentrations than this RPE action.

The electro-oculographic responses to alcohol and light in a series of patients with retinitis pigmentosa.

PURPOSE: Alcohol produces changes in the electro-oculogram (EOG) similar to those caused by light, but indirect evidence indicates that alcohol directly affects the retinal pigment epithelium (RPE). An investigation of the alcohol-induced increase (termed the alcohol rise in this study) in patients with disease of the photoreceptors was therefore of interest. METHODS: Standard EOGs were recorded after oral administration of alcohol in a group of patients with retinitis pigmentosa (RP). RESULTS: The average response of 17 patients to alcohol was a slow decrease of potential, which contrasts with the normal alcohol rise. In patients with considerable residual peripheral field, alcohol produced a small increase of voltage, followed by a prolonged decrease. The slower decrease in the EOG voltage was evident in patients with small fields and could be seen even in those who had lost all visual function. Light caused small increments of EOG voltage (termed light rises), again related to the field size. CONCLUSIONS: It is probable that the intracellular signaling system that causes the alcohol and light rises is lost in RP.