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Mark Brinton, Jae Lim Chung, Andrea Kossler, Jim Loudin, Christopher Ta, Daniel V Palanker; Electrical Stimulation of the Lacrimal Gland in Rabbits. Invest. Ophthalmol. Vis. Sci. 2014;55(13):50.
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Electrical stimulation of the lacrimal gland is a promising new approach to increase tear production and provide relief to patients afflicted by dry eye disease. Delivery of electrical pulses via implanted electrodes increases tear production; however, it is unknown whether electrical stimulation directly affects acinar cells in the gland, or if it engages sympathetic or parasympathetic neurons. Understanding the pathways is essential for development of an efficient stimulation protocol and electrode configuration.
New Zealand White rabbits were anesthetized using isoflurane inhalation and implanted with 3-mm diameter bipolar platinum disc electrodes, spaced 10mm apart, beneath the inferior lacrimal gland. Baseline and stimulated tear production was measured using 3-mm wide Schirmer strips for 5 minutes. Symmetric biphasic pulses of current (0.5ms duration at 30Hz) were applied from a custom pulse generator throughout the 5-minute Schirmer test. To determine the pathways of the tearing response to stimulation the animals were given parasympathetic (scopolamine) and sympathetic (prazosin and phenoxybenzamine) blockers prior to electrical stimulation.
Electrical stimulation caused an increase in Schirmer test scores from the 2 mm baseline by 6 and 10 mm for the 6 and 12-mA pulses, respectively. Schirmer tests from the fellow eye suggest little or no bilateral effect. Administration of scopolamine reduced the effect of the 6-mA electrical stimulation to < 1mm above baseline for 90 minutes, after which the elicited tearing response returned to original level. The sympathetic alpha blockers, prazosin and phenoxybenzamine, did not affect stimulated tear production.
Electrical stimulation of the lacrimal gland can increase tear production by several fold (3-5), depending on the pulse parameters. However, excessive stimulation can engage undesired nerve fibers, including muscle twitching observed with 12-mA stimulation. The elimination of the stimulated tearing effect with parasympathetic blockers indicates that the response does not originate in the acinar cells of the gland, but is rather mediated by neural stimulation. That the sympathetic nerve blockers did not affect tear response suggests that electrical stimulation engages efferent parasympathetic fibers in the gland to enhance tear production.
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