| Purpose Retinal ischemic insult is one of common ophthalmic clinic manifestations. There are many causes, such as obstructive retinopathies, venous capillary insufficiency, diabetic retinopathy; anomalous occular shunts,hypertensive retinopathy, retinal neovascularization, retinal detatchment and vitreous hemorrhage, and so on. In addition, vitrectomy and retinal detachment surgery, which can reduce retinal blood flow, can result in retinal ischemic insult. The retina is part of the central nervous system (CNS) and many neurological diseases accompany with retinal diseases. Recently, exprimental data indicate that excitatory amino acids (EAAs) -glutamate (Glu) can trigger excitotoxic insult. EAAs released during brain ischemia, which may be involved in hypoxic-ischemic brain injury. Moreover, some researchers also find that EAAs involved in the mechanism of retinal ischemia insult, and a 2-adrenoceptor agonists are neruropretective in ischemic insult. However, the neuroprotective effects and mechanism of a 2-adrenoceptor agonistsremain unclear.In this experiment, transient retinal ischemia was induced in rabbits by raising intraocular pressure. Before ischemia rabbits were injected intraperitoneally chlonidine hydrochloride ( 0.5mg/kg wt) , we compared the control and treatment groups by studying the retinal elctrophysiological, histological, and vitreal glutamate changes 1 hour, Iday, and 3 day after retinal ischemia. So we will further confirm clonidine's neuroprotective effects and mechanism.Method Twenty healthy adult rabbits (forty eyes) were randomly divided into two groups, control and treatment groups, and the treatment group were injected intraperitoneally clonidine hydrochloride ( 0.5mg/kg wt ) before ischemia. Elevating the intraocular pressure in all right eyes produced the retinal ischemia, and the left eyes were sham-operated. We examed the retinal electrophysiology of both eyes before and after ischemia, histology of rabbit retina 1 day and 3 day after ischemia, analyzed vitreous humor glutamate levels between control and clonidine-treated eyes, and compared results in different time. Result 1. Electrophysiological examination show significant reduction of ERG b-wave amplitude in right eyes of control group (P<0.05) , although there are gradual recovery 1 day and 3 day after ischemia, the amplitude is still significantly lower than that before ischemia. There is no significant reduction of b-wave amplitude in right eyes except 1 hour after ischemia compared with left eyes in treatment groups. In addition, the amplitude of 30 Hz flicker ERGs didn't significantly reduced in both groups (P>0.05) , although it has a mild reduction after ischemia.2. Retinal histological section examination show inner nuclear layer, inner plexiform layer and ganglion fiber layer became significantly thinner 1 day and 3 day after ischemia than those before ischemia (P<0.05) , but the ganglion fiber layer's thickness didn't significantly reduced 1 hour after ischemia because mild edema (P>0.05) . Meanwhile the ganglion cell count became decreased after ischemia (P<0.05) . The inner nuclear layer cells and ganglion cells became disordered. On the contrary, there is significant difference between right and left eyes in treatment group, also between right eyes of control and treatmentgroups except the ganglion fiber layer thickness after 1 hour after ischemia (P<0.05) .3. Vitreous humor glutamate analysis show the right eye vitreous glutamate concentration significantly increased compared with left eyes in control group 1 day and 3 day after ischemia (P<0.05) , and much higher hi 3 day after ischemia which may be caused by the death of retinal neural cells hi which the glutamate leaked into extracellular space. The vitreal glutamate didn't significantly increase in treatment group, though it mildly increased in 3 day after ischemia.Conclusion 1. a 2-adrenoceptor agonist-clonidine hydrochloride can protect retinal structure in acute ischemia insult, which can attenuate inner layer insult by preventing...
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