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BACKGROUND: Following trauma caused by seawater, cells often exhibit special pathological changes because of the special physico-chemical properties of seawater.OBJECTIVE: To observe corneal histopathological changes and interleukin-6 level in aqueous humor of a rabbit model of penetrating corneal trauma combined with seawater immersion.METHODS: The rabbit eye models of penetrating corneal trauma caused by firecrackers were established in 16 adult healthy grey rabbits. A 3-mm whole-layer incision was made in the cornea. The right eyes served as experimental sides and the left eyes served as controls. Seawater was injected into the aqueous humor of the right eyes via the corneal incision. The eye surface was flushed with seawater for 30 minutes. Physiological saline was used for the left eyes. RESULTS AND CONCLUSION: Optical microscopy results showed that at 1, 2, 3 days after model establishment, corneal cells on the experimental side exhibited severe necrosis and abscission, obvious swelling of substantia propria layer complicated by cellular infiltration. At 1 and 2 days after model establishment, the pathological changes on the control side were the same as the experimental side, but they were mild, but at 3 and 5 days, they were obviously alleviated. At 1, 2, 3 days after model establishment, interleukin-6 level in aqueous humor was significantly higher on the experimental side than on the control side (P < 0.05). These findings suggest that the degree of injury on the experimental side was more severe than that on the control side, indicating that seawater may be an important causative factor of corneal injury.
ABSTRACT
Background Researches have demonstrated that ocular hypertension induces the ischemia-reperfusion of retina and further leads to the degeneration of retinal ganglion cells,but its mechanism is beyond understanding.Objective The present study aims to observe the effects of static pressure on the morphology,proliferation activity and viability of cultured retinal microvascular endothelial cells (RMECs) and evaluate the expression of ET-1 and NO in these cells under variant static pressure.Methods RMECs were isolated from 30 healthy Wistar rats and cultured using explant culture method by Ⅷ factor antibody and PECAM-1 antibody.The static pressure of 1.33kPa,2.67kPa,5.33kPa and 10.67kPa was used in culture bottle respectively.The RMECs without static pressure were used as normal control group.The morphology of RMECs under the different static pressure was observed by inverted phase contrast microscopy,and the number of RMECs was counted using the counting plate.Cellular viability was studied by trypan blue staining.The changes of ET-1 and NO_2~-/NO_3~-,two metabolic products of NO,in the medium were detected by radioimmunoassay and Griess's nitrate reductase method.The expression of ET-1,eNOS and iNOS mRNA in RMECs was analyzed by semi-quantitative RT-PCR 24 hours after treatment of variant static pressure.Results Cultured RMECs sticked well at 24 hours and reached to confluence at 48 hours and showed the red fluorescence for Ⅷ factor antibody and PECAM-1 antibody.Enlargement of nuclei,extenders of cell bodies and suspension of RMECs in medium were observed.The number of RMECs was gradually increased.The cell viability was reduced with the raise of static pressure among these four groups(F=12.205,P＜0.01;F=11.180,P＜0.01).The static pressure increased the content of ET-1 released by RMECs in 2.67kPa,5.33kPa and 10.67kPa of static pressure groups,and concentrations of NO_2~-/NO_3~- in the medium showed a significant increase in 5.33kPa and 10.67kPa of static pressure groups compared with normal and 1.33kPa of static pressure groups(P＜0.01).The expressions of ET-1 mRNA,eNOS mRNA and iNOS mRNA were considerably enhanced in 5.33kPa and 10.67kPa of static pressure groups compared with normal control group(P＜0.01).Conclusion Raised static pressure causes the alteration of RMGCs structure and morphology.Static pressure could upregulate the expressions of ET-1,eNOS and iNOS mRNA in RMECs and increase the release of ET-1 and NO.This pathway might be one of pathologic mechanisms of retinal injury induced by high intraocular pressure.
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To investigate the role of intercellular adhesion molecule 1(ICAM 1) in the pathogenesis of bacterial keratitis,22 rats were randomly divided into bacterial keratitis group and control group. A specific staining of corneal epithelial cells, stromal keratocytes and endothelial cells for ICAM 1 was carried out by using monoclonal antibody to ICAM 1 and immunohistochemical staining techniques. The results showed that ICAM 1 expressed a low level in the corneal epithelial cells, stromal keratocytes and endothelial cells in the control group(-~+), while its expression was strong in the keratitis group (~). The difference between two groups was statistically significant ( P
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To evaluate the efficacy of intravenous administration of aminocaproic acid in pre-venting secondary hemorrhage after traumatic hyphemas. Methods: 60 patients with traumatic hyphemaswere random separated into two groups: (1 ) Routine treated group: 31 patients received intramuscular ad-ministration of adrenosin or dicynone and oral administration of steroids t (2) Arninocaproic acid treatedgroup: 29 patients received aminocaproic acid in an intravenous drip. Results: The incidence of secondaryhemorrhage in the amin0caproic acid treated group was much lower than that in the routine treated group(P