ArticleDocumenta ophthalmologica. Advances in ophthalmology2002
Nitric oxide and octreotide in retinal ischemia-reperfusion injury.
Article in Documenta ophthalmologica. Advances in ophthalmology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 19 citations in OpenAlex.
- Octreotide Protects the Mouse Retina against Ischemic Reperfusion Injury through Regulation of Antioxidation and Activation of NF-κB.Oxidative medicine and cellular longevity · 2015Article
- Role of somatostatin receptor-2 in gentamicin-induced auditory hair cell loss in the Mammalian inner ear.PloS one · 2014Article
- The impact of octreotide in experimental proliferative vitreoretinopathy.Indian journal of ophthalmology · 2013Article
- The somatostatinergic system in the mammalian cochlea.BMC neuroscience · 2011Article
- The effect of GABA and the GABA-uptake-blocker NO-711 on the b-wave of the ERG and the responses of horizontal cells to light.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2004Article
- The effect of octreotide against oxidative damage in photosensitized conjunctiva and cornea of rabbits.Documenta ophthalmologica. Advances in ophthalmologyArticle
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Authors and funding
2 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
This experimental study was performed to investigate the role of ischemia-reperfusion injury on retinal nitric oxide activity and to determine whether octreotide, the synthetic analogue of natural somatostatin, modifies the nitric oxide activity during retinal ischemia-reperfusion in a quinea pig model. Three groups of seven pigmented male quinea pigs were formed; Control, Ischemia and the Ischemia/Octreotide groups. 90 minutes of pressure-induced retinal ischemia and 24 h of reperfusion were established in the ischemia and ischemia/octreotide groups. Saline for the ischemia group and 50 microg/kg of octreotide for the ischemia/octreotide group were administered intraperitoneally five times with 6-h intervals. At the end of the reperfusion period both eyes of the animals of the three groups were enucleated. One eye of each animal was randomly selected for biochemical assay and the other for histopathological analysis. Retinal nitrate levels were measured and histopathological changes were evaluated in the groups. The mean retinal nitrate levels of the control, ischemia and ischemia/octreotide groups were 157.6 +/- 25.2, 106.4 +/- 20.1 and 96.4 +/- 17.7 micromol/l, respectively. Nitrate levels decreased significantly both in the ischemia (p < 0.01) and ischemia/octreotide (p < 0.01) groups versus control. In the ischemia group, retinal histopathological changes, which were different from the control group, were prominent edema, polymorphonucleated leukocytes infiltration and vacuolated spaces in the inner retina. No significant change was observed in the histopathological specimens of the ischemia/octreotide group. Significant increase in the thickness of the inner plexiform layer of the retina of the ischemia group was observed versus the control and ischemia/octreotide groups (p < 0.01 and p < 0.01, respectively). The thickness of the inner plexiform layer of the retina of the ischemia/octreotide group did not change versus the control group. It was concluded that nitric oxide activity decreased during retinal ischemia-reperfusion and, although octreotide prevented the histopathological damage, it could not ameliorate the nitric oxide activity of the retina.
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