An amperometric needle-type electrochemical glucose sensor intended for tear glucose measurements is described and employed in conjunction with a 0.84 mm i.d. capillary tube to collect microliter volumes of tear fluid. The sensor is based on immobilizing glucose oxidase on a 0.25 mm o.d. platinum/iridium (Pt/Ir) wire and anodically detecting the liberated hydrogen peroxide from the enzymatic reaction. Inner layers of Nafion and an electropolymerized film of 1,3-diaminobenzene/resorcinol greatly enhance the selectivity for glucose over potential interferences in tear fluid, including ascorbic acid and uric acid. Further, the new sensor is optimized to achieve very low detection limits of 1.5 ± 0.4 μM of glucose (S/N = 3) that is required to monitor glucose levels in tear fluid with a glucose sensitivity of 0.032 ± 0.02 nA/μM (n = 6). Only 4-5 μL of tear fluid in the capillary tube is required when the needle sensor is inserted into the capillary. The glucose sensor was employed to measure tear glucose levels in anesthetized rabbits over an 8 h period while also measuring the blood glucose values. A strong correlation between tear and blood glucose levels was found, suggesting that measurement of tear glucose is a potential noninvasive substitute for blood glucose measurements, and the new sensor configuration could aid in conducting further research in this direction.
Tear glucose measurements have been suggested as a potential alternative to blood glucose monitoring for diabetic patients. While previous work has reported that there is a correlation between blood and tear glucose levels in humans, this link has not been thoroughly established and additional clinical studies are needed. Herein, we evaluate the potential of using commercial blood glucose test strips to measure glucose in tears. Of several blood glucose strips evaluated, only one brand exhibits the low detection limit required for quantitating glucose in tears. Calibration of these strips in the range of 0-100 μM glucose with an applied potential of 150 mV to the working electrode yields a sensitivity of 0.127 nA/μM and a limit of quantitation (LOQ) of 9 μM. The strips also exhibit ≤13% error (n = 3) for 25, 50, and 75 μM glucose in the presence of 10 μM acetaminophen, 100 μM ascorbic acid, and 100 μM uric acid. Measurements of glucose in tears from nine normal (nondiabetic) fasting human subjects using strips yielded glucose values within the range of 5-148 μM (mean = 47 μM, median = 43 μM), similar to those for human tears reported by others with more complex LC-MS methods. The glucometer strip method could facilitate more clinical studies to determine whether tear glucose and blood glucose levels sufficiently correlate for application to routine measurements in tears to supplement blood glucose testing. This would be especially helpful for children, adolescents, other Type 1 diabetics, and also for Type 2 diabetics who require treatment with insulin and cannot tolerate multiple finger sticks per day.
This study describes a dramatic rise in intraocular pressure which occurs within a few hours after cataract surgery without the use of a-chymotrypsin. Early reports stated that intraocular pressures remained low after cataract surgery, but these statements were based on measurements made several days (Hilding, I955) or weeks after surgery (Miller, Keskey, and Becker, 1957). Applanation measurements made I2 hours after surgery were reported at or below the preoperative level (Galin, Baras, and Perry, I96I). Gormaz (i962, 1973) first reported ocular hypertension one day after cataract surgery and did not use oc-chymotrypsin. Giardini and Paliaga (I964) reported ocular hypertension 8 hours after cataract surgery with a technique which included the use of oc-chymotrypsin. The association of this enzyme with a postoperative rise in intraocular pressure was made by Kirsch (I964). Galin, Barasch, and Harris (I966) supported this relationship. However, in those eyes in which o-chymotrypsin had not been used, Kirsch (I964) reported a 23 per cent. and Galin and others (I966) an 8 per cent. incidence of ocular hypertension, by their criteria. Rich ( I 968) demonstrated a consistent rise in intraocular pressure one day after cataract surgery without the use of a-chymotrypsin and with a technique designed to secure water-tight incision closure. He suggested that an early postoperative rise in intraocular pressure followed all cases of cataract surgery in which incision closure was water-tight. MethodsCataract surgery was performed on ten consecutive patients (Cases i to I o) whose eyes were otherwise normal. The age range was 54 to 86 yrs. Preoperative preparation of the patient included one drop of a steroid-antibiotic combination the night before and on the morning of surgery. Preoperative sedation was intramuscular diazepam IO mg. one hour before surgery. No mydriatic or other medication, local or systemic, was used. The operations were performed under local anaesthesia with topical proparacaine o-s per cent. and facial nerve block and retrobulbar anaesthesia with lignocaine 2 per cent. with adrenaline i :iooo and hyaluronidase. The operations were performed by the same surgeon using a surgical microscope.The anterior chamber was entered beneath a limbus-based conjunctival flap through a bevelled comeo-scleral incision; the outer two-thirds of this incision were vertical and the inner portion sharply angled anteriorly. Two corneo-scleral sutures of 25 p diameter Perlon were placed before the chamber was entered. The lens was removed by cryoextraction. a-chymotrypsin was not used. The anterior chamber was then irrigated with a I in 200 solution of acetylcholine, the corneo-scleral sutures were tied, and a basal iridectomy was performed. The corneo-scleral incision was additionally
In addition to the application of this imaging method to studies of the effect on optic disc cupping of induced increased intraocular pressure in rats and mice, by detecting and documenting the onset and the course of optic neuropathy, it should be valuable in identifying animal models of glaucoma, in studying neuropathogenic mechanisms, and in assessing the effects of experimental therapies.
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