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  • Author or Editor: Elizabeth J. Galbreath x
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SUMMARY

Objective

To examine the role of apoptosis in retinal photoreceptor degeneration in dogs with sudden acquired retinal degeneration syndrome (SARDS).

Sample Population

Retinas from 3 dogs with SARDS and from 2 clinically normal adult dogs.

Procedure

Apoptosis was identified by in situ endlabeling and observation of characteristic morphologic changes by light microscopy.

Results

The degree of photoreceptor degeneration varied with duration of vision loss in SARDS-affected eyes. The retina of all 3 SARDS-affected eyes had numerous (34, 61, and 70) apoptotic nuclei per section that were overwhelmingly located in the outer nuclear layer. Apoptotic nuclei were not detected, or were rare in similarly sized retinal sections from normal dogs. Inflammation was not an important feature of SARDS.

Conclusions

Apoptosis appears to be at least 1 mechanism of photoreceptor cell death in dogs with SARDS.

Clinical Relevance

Because apoptosis appears to be a final common pathway in many retinal degeneration syndromes, future treatment strategies that control apoptosis in other diseases may be applicable to dogs with SARDS. Halting this pathway may allow some photoreceptors to survive and, perhaps, preserve vision. (Am J Vet Res 1998;59:149–152)

Free access
in American Journal of Veterinary Research

Summary

Intestinal ischemia was induced and maintained for 60 minutes in male Sprague-Dawley rats weighing 175 to 225 g. Prior to reperfusion, the following drugs were administered via the caudal vena cava: 0.9% NaCl (0.5 ml), superoxide dismutase (sod; 1,000 IU/kg of body weight), polyethylene glycol-conjugated sod (peg-sod; 1,000 IU/kg), or the 21-aminosteroids, U74006F (3 mg/kg) or U78715G (3 mg/kg). A sham-operated control group was included. Animals from each group were euthanatized at 5 periods of reperfusion: 5 minutes, 30 minutes, 18 hours, 3 days, and 7 days after reperfusion. Fixed tissues were embedded in paraffin, sectioned at 5 μm, and stained with H&E. Villi profiled in cross section were measured from the crypt villus junction to the tip of the villus. The mean villus height for each rat was calculated and compared by two-way anova to determine the effects of time and treatment.

Villus height was maintained after 30 minutes of reperfusion in rats of the sham- and U74006F-treated groups; U78715G and sod treatment attentuated the loss in villus height, and villus height was not maintained in the peg-sod- and 0.9% NaCl-treated rats. In all rats, villus height was comparable to, or was greater than villus height in sham-operated controls by 18 hours after reperfusion in all animals and remained constant through 7 days.

Administration of the 21-aminosteroids maintained villus height after ischemia and reperfusion. Treatment with peg-sod did not maintain villus height to the degree observed in rats treated with sod.

Free access
in American Journal of Veterinary Research