An experimental study of quinine blindness

Abstract

SummaryAn experimental model of qumme induced blindness is presented. Elec trophysiological, angiographical and morphological examinations were made. The occurrence of blindness and any recovery from blindness was dependent upon the dose of quinine taken. As no evidence of acute retinal ischaemia was found it is concluded that quinine is retinotoxic.Despite the many clinicaP and experimentaF reports of quinine blindness providing much detailed evidence and analysis, the first line of clinical therapy continues to be directed at preventing retinal vasoconstriction either using vasodilator drugs or interfering with the sympathetic nerve supply by blocking a stell ate ganglion.3,4 Our experiment was designed to create an animal model which would allow us to study the genesis of quinine blindness electrophysiologically, fluorescein angio graphically and morphologically. Our inten tion was that by correlating these findings we might identify the site and mode of action of quinine, so that rational therapeutic regimens could be designed and tested. We present some of our preliminary observations. Additional observations included blood pressure, heart rate and respiratory rate. All observations and recordings were made at half hourly intervals.Fourteen cats were anaesthetised and ERG and VER recordings were made to determine the normal range of the ERG A and B waves and the morphology of the VER (Fig. 1). The cats were allowed to recover and at a later date were given oral doses of quinine sulphate. After 2 hours they were anaesthetised and observations commenced.During the acute experiments, when quinine was given, flourescein angiography was performed on the right eye.After the acute experiment the cats were allowed

The effects of hypoxia on the ERG in paediatric cerebral malaria

“…[12][13][14][15] Elapsed time from most recently administered quinine infusion (QET) was measured. A significant positive association was found between QET and both maximal-response a wave amplitude (P ¼ 0.03) and cone a wave amplitude (P ¼ 0.04).…”

Cancer-Associated Retinopathy

“…This product has yet to be defined (to our knowledge) and may be released in small concen¬ trations but must be capable of induc¬ ing strong "hormonelike" effects when bound to the appropriate recep¬ tor. 11 The second theory relates to the possibility of autoimmune reactions triggered by the host's response to tumor antigens that cross-react with specific retinal components. Several investigators have reported the pro¬ duction of antiretina immunoglobu¬ lins in patients with cancer1416 and demonstrated immune reactions by the serum samples of patients with CAR to in vitro cultivated lung cancer cells.…”

Treatment with chloroquine is retinotoxic in captive African penguins (Speniscus demersus). Attenuation and recovery of electroretinographic responses

“…The exact mechanism by which CQ and HCQ cause retinal toxicity is yet to be determined. Data from in‐vitro and animal model studies suggest that the drugs accumulate in RPE cells, inhibit the recycling of all‐trans‐retinol and might result in photoreceptor degeneration 3,29 . However, recent data from SD‐OCT scans in humans suggest an alternative sequence of events in which the primary site of toxicity is the photoreceptor layer, with secondary effect on RPE cells 30 …”