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(Investigative Ophthalmology and Visual Science. 2000;41:2697-2701.)
© 2000 by The Association for Research in Vision and Ophthalmology, Inc.

The Effect of Calcium Channel Blocker Diltiazem on Photoreceptor Degeneration in the Rhodopsin Pro23His Rat

Ronald A. Bush, Laureen Kononen, Shigeki Machida and Paul A. Sieving

From the Department of Ophthalmology and Visual Sciences, University of Michigan, Ann Arbor, Michigan.

PURPOSE. To determine whether the calcium channel blocker D-cis-diltiazem promotes photoreceptor survival in rats with the Pro23His rhodopsin mutation.

METHODS. Heterozygous Pro23His rhodopsin line 1 rats (n = 11) were treated daily, according to a protocol applied successfully in rd mice, with D-cis-diltiazem hydrochloride increased incrementally from 21 to 54 mg/kg in a divided dose (8 AM and 8 PM) administered by intraperitoneal (IP) injection for 21 days, beginning on days of age 10 through 12. Saline-treated line 1 rats (n = 6) received IP injections of an equal volume of 0.9% saline. Analysis on day 35 of age included dark-adapted corneal electroretinogram (ERG) b- and a-waves recorded from threshold to 0.63 log candela-seconds [cd-s]/m2, saturated a-waves elicited with a 2.1 log cd-s/m2 flash, and morphometry of the outer nuclear layer (ONL) and rod outer segments (ROS).

RESULTS. ONL width and cell counts of diltiazem-treated and saline-treated animals at 35 days were reduced to 64%–68% of 15-day-old untreated P23H line 1 retinas. No photoreceptor rescue was found by measuring ONL width (P = 0.84), cell count (P = 0.42), or ROS length (P = 0.85). Functional assays by ERG b-wave threshold (P = 0.57), b-wave maximum amplitude (P = 0.46), and saturated a-wave amplitude (P = 0.59) also showed no rescue.

CONCLUSIONS. D-cis-Diltiazem did not rescue photoreceptors of Pro23His rhodopsin mutation line 1 rats treated according to the protocol used in rd mouse.




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