Quantitation of ischemic damage in the rat retina

Hughes, William F.

doi:10.1016/0014-4835(91)90215-z

Cited by 217 publications

(151 citation statements)

References 24 publications

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“…Schmidt-Schönbein and colleagues [14] have shown the mechanism by which leukocyte adhesion occurs in a postcapillary vessel, and it is now widely accepted that leukocyte adhesion frequently occurs during postischemic reperfusion. In the rat retina, serious edema develops following 90-min ischemia, moderate edema following 60-min ischemia, but no edema after 30-min ischemia [11]. The present study also demonstrated that 120-min ischemia with 40-50% of normal blood flow produced remarkable edema in young rats.…”

Section: Discussionsupporting

confidence: 61%

“…The cells reduce their metabolic activities if they get injured, which in turn may decrease the regional blood flow. Hughes [11] examined the threshold for cellular injury in the rat retina and demonstrated that extensive damage of the inner and outer retinae was observed only after 60 and 90 min of no-flow ischemia, respectively. Reinecke and coworkers [12] also suggested that the retina subjected to an ischemic period of 90 min suffers tissue damage, showing loss of ganglion cells, rods, cones, and bipolar cells.…”

Section: Discussionmentioning

confidence: 99%

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Postischemic Reperfusion in the Eyes of Young and Aged Rats.

Ishihara¹,

Nakano²,

Ohama³

et al. 2000

JJP

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The hemodynamics during postischemic reperfusion are complex and not yet fully understood. Hyperperfusion followed by delayed hypoperfusion is often observed during the reperfusion period after ischemia in the brain [1]. In the eye, the hyperemic response during the early phase of reperfusion is well documented. Roth and Pietrzyk [2] demonstrated hyperperfusion after 1 h of retinal ischemia in cats. We showed that the magnitude of postischemic hyperperfusion was greater after 30-min ischemia than after 10-min ischemia in the eyes of rats [3]. The magnitude of hyperperfusion was smaller after 50-min ischemia than after 30-min ischemia, although the difference between the two groups was not statistically significant.It is worthwhile to know the effect of longer periods of ischemia on hyperperfusion. Thus, the first purpose in the present study was to compare hyperperfusion after 30-min ocular ischemia with that after 120 min.Although Roth and Pietrzyk [2] reported that delayed hypoperfusion did not occur during the reperfusion period after 1-h ischemia in cats, it may be induced after longer periods of ischemia. Traupe and coworkers [1] showed that brain ischemia lasting 60 min or more in cats induced delayed hypoperfusion which could exacerbate ischemic damage. The second purpose, therefore, was to examine whether 120-min ocular ischemia would cause delayed hypoperfusion and investigate the retinal histological changes during Key words: ischemia-reperfusion, choroidal blood flow, aging, intraocular pressure, edema. Abstract:The hemodynamic changes during postischemic reperfusion were investigated in the eyes of young (4 months) and aged (more than 18 months) rats using laser Doppler flowmetry, and histological changes in the retina were examined 6 h after the cessation of ischemia. During exposure to 80 mmHg of intraocular pressure, choroidal blood flow (ChBF) decreased to 40-50% of the baseline value. Marked hyperperfusion (186Ϯ9%) was observed 1 min after cessation of 30-min ischemia in young rats. The hyperperfusion was less (111Ϯ3%) after 120-min ischemia. Delayed hypoperfusion was not observed during 6 h of reperfusion after 120-min ischemia. In aged rats, the hyperperfusion after 30-min ischemia was less (130Ϯ17%) than that in young rats, and the ChBF decreased to 80% of the baseline value during 6 h of reperfusion after 120-min ischemia. Histological examination of the retina showed that exposure to 120-min ischemia caused microvacuolation in the inner and outer plexiform layers and vacuolar changes in the cytoplasms in the inner nuclear layer of both young and aged rats, suggesting edema formation in the retina. The thickness of the outer layers of the retina tended to increase after 120-min ischemia in young rats, whereas it decreased significantly in aged rats. These results suggest that 120-min ischemia with 40-50% of normal choroidal blood flow causes more severe damage than 30-min ischemia, and that the hemodynamic changes during reperfusion in aged rats are different from those in young rats.

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Section: Discussionsupporting

confidence: 61%

Section: Discussionmentioning

confidence: 99%

Postischemic Reperfusion in the Eyes of Young and Aged Rats.

Ishihara¹,

Nakano²,

Ohama³

et al. 2000

JJP

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“…Five visual fields were sampled from the posterior portion of each retina using a 40 ϫ objective (each visual field representing a 340 m length of retina). Within each visual field, the thickness of the inner plexiform layer, inner nuclear layer, and entire retina (excluding photoreceptors) was measured by the method of Hughes (25). To compensate for any bias due to skewed sectioning angle (i.e., deviation from 90 Њ ), all measurements were expressed relative to the thickness of the choroid in the respective section.…”

Section: Methodsmentioning

confidence: 99%

Neural apoptosis in the retina during experimental and human diabetes. Early onset and effect of insulin.

Barber

Lieth²,

Khin³

et al. 1998

J. Clin. Invest.

1,126

902

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This study determined whether retinal degeneration during diabetes includes retinal neural cell apoptosis. Image analysis of retinal sections from streptozotocin (STZ) diabetic rats after 7.5 months of STZ diabetes identified 22% and 14% reductions in the thickness of the inner plexiform and inner nuclear layers, respectively ( P Ͻ 0.001). The number of surviving ganglion cells was also reduced by 10% compared to controls ( P Ͻ 0.001). In situ end labeling of DNA terminal dUTP nick end labeling (TUNEL) identified a 10-fold increase in the frequency of retinal apoptosis in wholemounted rat retinas after 1, 3, 6, and 12 months of diabetes ( P Ͻ 0.001, P Ͻ 0.001, P Ͻ 0.01, and P Ͻ 0.01, respectively).

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“…In the histological examination of the retina, this procedure was found to cause retinal da mage through different types of cell death mechanisms such as apoptosis, necrosis, and nonlysosomal vesiculate (5) . Hughes demonstrated increased apoptosis and INL thinning in a tissue model of acute ischemic injury (30) . In addition, a number of investigations have shown that a peak in apoptosis occurs 6 to 18 h after I/R, returning to control levels after 48 h (31,32) .…”

Section: Discussionmentioning

confidence: 98%

Quercetin protects the retina by reducing apoptosis due to ischemia-reperfusion injury in a rat model

Arıkan¹,

Erşan²,

Karaca³

et al. 2015

Arquivos Brasileiros De Oftalmologia

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Purpose: This study aimed to investigate the effect of quercetin on apoptotic cell death induced by ischemia-reperfusion (I/R) injury in the rat retina. Methods: Twenty-four rats were divided into four equal groups: control, ischemic, solvent, and quercetin. I/R injury was achieved by elevating the intraocular pressure above the perfusion pressure. Intraperitoneal injections of 20 mg/kg of quercetin and dimethyl sulfoxide (DMSO) were performed in the quercetin and solvent groups, respectively, immediately prior to I/R injury, and the researchers allowed for the retinas to be reperfused. Forty-eight hours after injury, the thicknesses of the retinal ganglion cell layer (RGCL), inner nuclear layer (INL), inner plexiform layer (IPL), outer plexiform layer (OPL), and outer nuclear layer (ONL) were measured in all groups. Moreover, the numbers of terminal deoxynucleotidyl transferase dUTP nick-end-labeled [TUNEL (+)] cells and caspase-3 (+) cells in both INL and ONL were evaluated in all groups. Results: The administration of quercetin was found to reduce the thinning of all retinal layers. The mean thickness of INL in the quercetin and ischemic groups was 21 ± 5.6 µm and 16 ± 6.4 µm, respectively (P<0.05). Similarly, the mean thickness of ONL in the quercetin and ischemic groups was 50 ± 12.8 µm and 40 ± 8.7 µm, respectively (P<0.05). The antiapoptotic effect of quercetin in terms of reducing the numbers of both TUNEL (+) cells and caspase-3 (+) cells was significant in INL. The mean number of TUNEL (+) cells in INL in the ischemic and quercetin groups was 476.8 ± 45.6/mm 2 and 238.72 ± 251/mm², respectively (P<0.005). The mean number of caspase-3 (+) cells in INL of ischemic and quercetin groups was 633.6 ± 38.7/mm 2 and 342.4 ± 36.1/mm 2 , respectively (P<0.001). Conclusion:The use of quercetin may be beneficial in the treatment of retinal I/R injury because of its antiapoptotic effect on the retinal layers, particularly in INL.

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Quantitation of ischemic damage in the rat retina

Cited by 217 publications

References 24 publications

Postischemic Reperfusion in the Eyes of Young and Aged Rats.

Postischemic Reperfusion in the Eyes of Young and Aged Rats.

Neural apoptosis in the retina during experimental and human diabetes. Early onset and effect of insulin.

Quercetin protects the retina by reducing apoptosis due to ischemia-reperfusion injury in a rat model

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