Nitric oxide and octreotide in retinal ischemia-reperfusion injury

被引：20

作者：

Celiker U. ^{[1
]}

Ilhan N. ^{[2
]}

机构：

[1] Department of Ophthalmology, University Medical School, Elazig

[2] Department of Biochemistry, University Medical School, Elazig

来源：

Documenta Ophthalmologica | 2002年 / 105卷 / 3期

关键词：

Ischemia; Nitric oxide; Octreotide; Reperfusion; Retina;

D O I：

10.1023/A:1021243126512

中图分类号：

学科分类号：

摘要：

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 μg/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 μmol/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.

引用

页码：327 / 338

页数：11

共 49 条

[1]

Choi D.W., Glutamate neurotoxicity: A three stage process, Neurotoxicity of Amino Acids, pp. 235-242, (1991)

[2]

Goldstein I.M., Ostwald P., Roth S., Nitric oxide: A review of its role in retinal function and disease, Vision Res, 36, pp. 2979-2994, (1996)

[3]

Hangai M., Yoshimura N., Hiroi K., Mandai M., Honda Y., Inducible nitric oxide synthase in retinal ischemia-reperfusion injury, Exp Eye Res, 63, pp. 501-509, (1996)

[4]

Yamamato R., Bredt D.S., Snyder S.H., Stone R.A., The localization of nitric oxide synthase in rat eye and related cranial ganglia, Neuroscience, 54, pp. 19-200, (1993)

[5]

Koch K., Lambrecht H., Haberecht M., Redburn D., Schmith H.H.H.W., Functional coupling of a calcium/calmodulin-dependent nitric oxide synthase an a soluble quanyl cyclase in vertebrate photoreceptor cells, EMBO J, 13, pp. 3312-3320, (1994)

[6]

Perez M.T.R., Larsson B., Alm P., Anderson K.E., Ehinger B., Localization of neuronal nitric oxide synthase-immunoreactivity in rat and rabbit retinas, Brain Res, 104, pp. 207-217, (1995)

[7]

Chakravarty U., Stitt A.W., McNally J., Bailie J., Hoey E.M., Duprex P., Nitric oxide synthase activity and expression in retinal capillary endothelial cells and pericytes, Curr Eye Res, 14, pp. 285-294, (1994)

[8]

Goureau O., Hicks D., Courtois Y., De Kozak Y., Induction and regulation of nitric oxide synthase in retinal Müller glial cells, J Neurochem, 63, pp. 310-317, (1994)

[9]

Meyer P., Champion C., Schlotzer-Schrehardt U., Flammer J., Haefliger I.O., Localization of nitric oxide synthase isoforms in porcine ocular tissues, Curr Eye Res, 18, pp. 375-380, (1999)

[10]

Harrdy P., Dumont I., Bhattacharya M., Hou X., Lachapelle P., Varma D., Chemtob S., Oxidants, nitric oxide and prostanoids in the developing ocular vasculature: A basis for ischemic retinopathy, Cardiovasc Res, 47, pp. 489-509, (2000)

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