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Ronald A. Bush, Laureen Kononen, Shigeki Machida, Paul A. Sieving; The Effect of Calcium Channel Blocker Diltiazem on Photoreceptor Degeneration in the Rhodopsin Pro23His Rat. Invest. Ophthalmol. Vis. Sci. 2000;41(9):2697-2701.
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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
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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