Histological protection against ischemia–reperfusion injury by early ischemic preconditioning in rat retina

Sakamoto, Kenji; Yonoki, Yuzuru; Kuwagata, Mayumi; Saito, Maki; Nakahara, Tsutomu; Ishii, Kunio

doi:10.1016/j.brainres.2004.04.074

Cited by 35 publications

(19 citation statements)

References 21 publications

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“…A growing body of evidence indicates that the tissue injury observed after reperfusion is due to the reintroduction of oxygen rather than a delayed manifestation of injury caused by ischemia [31,35]. Up to now, various experimental designs have been described for the induction of ischemia-reperfusion damage in the retina, as vessel occlusion by clamping [1,8,9,13,24,28,30,32,33]. In the present study, we used the method of raising intraocular pressure above the arterial opening pressure.…”

Section: Discussionmentioning

confidence: 99%

“…In the other 4 groups (n=6), animals were treated with 0.9% NaCl, bimatoprost (Lumigan, Abdi Ibrahim Ilac Inc., Turkey), latanoprost (Xalatan, Pfizer Turkey Inc.), or travoprost (Travatan, Alcon Turkey Inc.) 1×1 drop/day for one week. At the end of one week, ischemia was created as described previously [9,30,33]. In short, animals were anesthesized with ketamine (50 mg/kg) and xylazine (5 mg/kg) and topical anesthetic was dropped on to the cornea of the animals.…”

Section: Experimental Model Of Ischemia and Reperfusionmentioning

confidence: 99%

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Comparison of the Protective Effects of Prostaglandin Analogues in the Ischemia and Reperfusion Model of Rabbit Eyes

et al. 2009

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This study was planned to investigate the neuroprotective potentials of three commercially available prostaglandin analogues (PGA), in the ischemia and reperfusion model (I/R). Thirty New Zealand rabbits were divided into 5 groups and except for the control group (non-ischemic, non-treated), 0.9% NaCl, bimatoprost, latanoprost, or travoprost were applied to both eyes of animals of the respective groups for 1 week. At the end of treatment, ischemia was induced in both eyes of the 4 treatment groups by anterior chamber irrigation of the animals for 60 min. Following 24 h reperfusion, the animals were sacrified. Enucleated eyes and retinal tissues were investigated by light microscopy, electron microscopy, immunohistochemicstry for retinal histopathology, intracellular and apoptotic cells and by retinal morphometry. Vitreous samples were biochemically investigated for probable role of reactive oxygen species, by measuring xanthine oxidase (XO) activity. Analysis of morphometric measurements and vitreous XO activity revealed significant differences between the PGAtreated groups and the NaCl-treated group (P<0.05). Similarly, apoptotic cell counts in different retinal layers showed that PGA-treated groups had fewer apoptotic cells in all retinal layers than the NaCl-treated ischemic group (P<0.05). PGA may have high protective potential for different retinal layers and cells. Biochemical analysis of vitreous showed that all PGAs decreased vitreous XO activity significantly compared to the NaCl-treated group (P<0.05). However we could not find any statistically significant differences among the analogues. PGAs may reduce the injury induced by I/R, through the inhibition of XO activity, and it seems that their effects are elicited through numerous pathways.

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Section: Discussionmentioning

confidence: 99%

Section: Experimental Model Of Ischemia and Reperfusionmentioning

confidence: 99%

Comparison of the Protective Effects of Prostaglandin Analogues in the Ischemia and Reperfusion Model of Rabbit Eyes

et al. 2009

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“…To test whether the anti-COX-2 antibody works well under our experimental conditions, we examined the immunoreactivity of COX-2 in rat retina at 6 h after induction of retinal ischemia. Retinal ischemia was induced by raising the intraocular pressure as reported previously (25). In brief, rats were anesthetized and the anterior chamber of the one eye, the pupil of which had been dilated with 1% atropine sulfate (Nihon Tenganyaku), was cannulated with a 27-gauge needle connected to a bottle filled with saline.…”

Section: Induction Of Retinal Ischemiamentioning

confidence: 99%

Nitric oxide dilates rat retinal blood vessels by cyclooxygenase-dependent mechanisms

Ogawa

Mori

Hasebe

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Ogawa N, Mori A, Hasebe M, Hoshino M, Saito M, Sakamoto K, Nakahara T, Ishii K. Nitric oxide dilates rat retinal blood vessels by cyclooxygenase-dependent mechanisms. Am J Physiol Regul Integr Comp Physiol 297: R968 -R977, 2009. First published July 22, 2009 doi:10.1152/ajpregu.91005.2008.-It has been suggested that nitric oxide (NO) stimulates the cyclooxygenase (COX)-dependent mechanisms in the ocular vasculature; however, the importance of the pathway in regulating retinal circulation in vivo remains to be elucidated. Therefore, we investigated the role of COX-dependent mechanisms in NO-induced vasodilation of retinal blood vessels in thiobutabarbital-anesthetized rats with and without neuronal blockade (tetrodotoxin treatment). Fundus images were captured with a digital camera that was equipped with a special objective lens. The retinal vascular response was assessed by measuring changes in diameter of the retinal blood vessel. The localization of COX and soluble guanylyl cyclase in rat retina was examined using immunohistochemistry. The NO donors (sodium nitroprusside and NOR3) increased the diameter of the retinal blood vessels but decreased systemic blood pressure in a dose-dependent manner. Treatment of rats with indomethacin, a nonselective COX inhibitor, or SC-560, a selective COX-1 inhibitor, markedly attenuated the vasodilation of retinal arterioles, but not the depressor response, to the NO donors. However, both the vascular responses to NO donors were unaffected by the selective COX-2 inhibitors NS-398 and nimesulide. Indomethacin did not change the retinal vascular and depressor responses to hydralazine, 8-(4-chlorophenylthio)-guanosine-3Ј, 5Ј-cyclic monophosphate (a membranepermeable cGMP analog) and 8-(4-chlorophenylthio)-adenosine-3Ј, 5Ј-cyclic monophosphate (a membrane-permeable cAMP analog). Treatment with SQ 22536, an adenylyl cyclase inhibitor, but not ODQ, a soluble guanylyl cyclase inhibitor, significantly attenuated the NOR3-induced vasodilation of retinal arterioles. The COX-1 immunoreactivity was found in retinal blood vessels. The retinal blood vessel was faintly stained for soluble guanylyl cyclase, although the apparent immunoreactivities on mesenteric and choroidal blood vessels were observed. These results suggest that NO exerts a substantial part of its dilatory effect via a mechanism that involves COX-1-dependent pathway in rat retinal vasculature. cyclooxygenases; prostaglandins; retinal blood vessel NITRIC OXIDE (NO) IS A POTENT vasodilator that activates soluble guanylyl cyclase (sGC), resulting in the elevation of intracellular cGMP in vascular smooth muscle cells, thereby dilating blood vessels in many organs (18). However, there is the evidence showing that cGMP-independent alternative/additional pathways are also involved. For example, NO directly activates the Ca 2ϩ

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“…Previous studies have reported that K ATP channels play an important role in enhancing retinal resistance against ischemic insult (10,12,14,26). Retinal ischemic injury induces cell death of retinal neurons by excitotoxicity.…”

Section: Discussionmentioning

confidence: 99%

KR-31378, a Potassium-Channel Opener, Induces the Protection of Retinal Ganglion Cells in Rat Retinal Ischemic Models

Choi¹,

Choi²,

Yoon³

et al. 2009

J Pharmacol Sci

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Abstract. KR-31378 is a newly developed K ATP -channel opener. To investigate the ability of KR-31378 to protect retinal ganglion cells (RGC), experiments were conducted using two retinal ischemia models. Retinal ischemia was induced by transient high intraocular pressure (IOP) for acute ischemia and by three episcleral vein occlusion for chronic retinal ischemia. KR-31378 was injected intraperitoneally and administered orally in the acute and chronic ischemia models, respectively. Under the condition of chronic ischemia, RGC density in the KR-31378-treated group was statistically higher than that in the non-treated group, and IOP was reduced. In the acute retinal ischemia model, 90% of RGC were degenerated after one week in non-treated retina, but, RGC in KR-31378-treated retina were protected from ischemic damage in a dosedependent manner and showed inhibited glial fibrillary acidic protein (GFAP) expression. Furthermore, the KR-31378 protective effect was inhibited by glibenclamide treatment in acute ischemia. These findings indicate that systemic KR-31378 treatment may protect against ischemic injury-induced ganglion cell loss in glaucoma.

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Histological protection against ischemia–reperfusion injury by early ischemic preconditioning in rat retina

Cited by 35 publications

References 21 publications

Comparison of the Protective Effects of Prostaglandin Analogues in the Ischemia and Reperfusion Model of Rabbit Eyes

Comparison of the Protective Effects of Prostaglandin Analogues in the Ischemia and Reperfusion Model of Rabbit Eyes

Nitric oxide dilates rat retinal blood vessels by cyclooxygenase-dependent mechanisms

KR-31378, a Potassium-Channel Opener, Induces the Protection of Retinal Ganglion Cells in Rat Retinal Ischemic Models

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