Objective To observe the protective effects of diazoxide-preconditioning on myocardial ischemiareperfusion injury of rats and discuss its possible mechanisms. Methods Fourteen healthy SD rats were randomly divided into two groups（7 each group）,In diazoxide-preconditioning group diazoxide was injected with the dosage of 12.5mg/kg through the vein,and in control group the media with the same amount was only given before ischemia. The left anterior descending branch was ligated for 2 hours. The heart was quickly excised after 2 hours reperfusion to be used for measurement of the quantity of malondialdehyde（MDA）, the activity of superoxide dismutase （SOD）, the size of myocardial infarct area, and the cell apoptosis and ultrastructure in ischemic area. Results Compared with the control group, the quantity of MDA,the percentage of the weight of myocardial infarct area/ischemic area, and the rate of cell apoptosis in the diazoxide-preconditioning group were greatly reduced （P〈0.05, 0. 01）. The damage of cell uhrastructure was obviously alleviated,Conclusion Diazoxide-preconditioning provides evident cardioprotective effect on the myocardial ischemia-reperfusion injury of rats.
Objective To observe the protective effects of diazoxide-preconditioning on myocardial ischemiareperfusion injury of rats and discuss its possible mechanisms. Methods Fourteen healthy SD rats were randomly divided into two groups（7 each group）,In diazoxide-preconditioning group diazoxide was injected with the dosage of 12.5mg/kg through the vein,and in control group the media with the same amount was only given before ischemia. The left anterior descending branch was ligated for 2 hours. The heart was quickly excised after 2 hours reperfusion to be used for measurement of the quantity of malondialdehyde（MDA）, the activity of superoxide dismutase （SOD）, the size of myocardial infarct area, and the cell apoptosis and ultrastructure in ischemic area. Results Compared with the control group, the quantity of MDA,the percentage of the weight of myocardial infarct area/ischemic area, and the rate of cell apoptosis in the diazoxide-preconditioning group were greatly reduced （P〈0.05, 0. 01）. The damage of cell uhrastructure was obviously alleviated,Conclusion Diazoxide-preconditioning provides evident cardioprotective effect on the myocardial ischemia-reperfusion injury of rats.
ObjectiveTo observe the short-term intraocular pressure changes of the affected eye after the implantation of dexamethasone vitreous implant (Ozurdex), and indirectly understand the tightness of the scleral perforation of the 22G implant device.MethodsThis is a prospective cohort design clinical observational study. From January 2018 to January 2020, 90 eyes (90 patients) who underwent vitreous Ozurdex implantation in the Department of Ophthalmology of Beijing Hospital were included in the study. There were 52 males (52 eyes), and 38 females (38 eyes); they were 14-79 years old. Forty-three eyes (43 patients) had retinal vein occlusion with macular edema, 29 eyes (29 patients) had uveitis with or without macular edema, 18 eyes (18 patients) had diabetic macular edema. All eyes underwent standard scleral tunnel vitreous cavity implantation Ozurdex treatment. The intraocular pressure was measured with a non-contact pneumatic tonometer 10 min before implantation (baseline) and 10, 30 min and 2, 24 h after implantation. The difference were compared between the intraocular pressure at different time points after implantation and the baseline. Wilcoxon signed rank test was used to compare intraocular pressure between baseline and different time points after implantation.ResultsThe average baseline intraocular pressure of the affected eye was 14.85 [interquartile range (IQR): 11.60, 17.63] mmHg (1 mmHg=0.133 kPa). The average intraocular pressure at 10, 30 and 2, 24 hours after implantation were 11.90 (IQR: 8.95, 16.30), 13.75 (IQR: 9.95, 16.80), 13.60 (IQR: 10.95, 17.20), and 14.65 (IQR: 12.20, 17.50) mmHg. Compared with the baseline intraocular pressure, the intraocular pressure decreased at 10 and 30 minutes after implantation, the difference was statistically significant (P＜0.001, P=0.002); the intraocular pressure difference was not statistically significant at 2, 24 h after implantation (P=0.140, 0.280).ConclusionsThere is a statistically significant difference in intraocular pressure reduction compared with the baseline in 10 and 30 minutes after vitreous implantation of Ozurdex, and there is no statistically significant difference between 2, 24 hours. This suggests that the 22G scleral puncture port of the preinstalled implant device cannot be completely closed immediately, and short-term intraocular pressure monitoring after implantation should be appropriately strengthened.