Objective To observe the effect of intraocular pressure（IOP）rapid fluctuations on rat ocular hemodynamics. Methods SD rat model with IOP rapid fluctuations was established. The IOP was decreased from 12 mm Hg (1 mm Hg=0.133 kPa) to 0 mm Hg within 1 s. 2 minutes later, the IOP was increased from 0 mm Hg to 12 mm Hg within 1 s. The anterior segment photos of rats were taken by slit lamp image analysis system when IOP at 12 mm Hg and 0 mm Hg, while the iris vessels diameter (VD) was measured. The peak systolic velocity (PSV), end diastolic velocity (EDV), mean velocity (MV), resistant index (RI), pulsatility index (PI) and VD of rats central retinal artery (CRA) and central retinal vein (CRV) were detected and analyzed using color Doppler ultrasonography before and 5, 10, 20, 60s after IOP fluctuations. Results The iris VD was (28.30plusmn;5.80) or (59.80plusmn;6.40) mu;m when the IOP was 12 or 0 mm Hg, respectively. Compared with each other, the difference was statistically significant (t=8.98, P＜0.01). When the IOP decreased rapidly, the VD of iris, CRA and CRV expanded immediately; PSV, EDV and MV increased immediately, then decreased slowly; RI and PI decreased immediately. The differences among different periods were statistically significant (P＜0.01). The change magnitudes of CRA were bigger than those of CRV. Conversely, when the IOP increased rapidly, the VD of iris, CRA and CRV reduced immediately; PSV, EDV and MV decreased immediately; RI and PI increased immediately. The differences among different periods were statistically significant (P＜0.01). Conclusion IOP rapid fluctuations can induce dramatic fluctuation of rat ocular hemodynamics.
ObjectiveTo observe the expression of glutamate (Glu) andγ-aminobutyric acid (GABA) in the retina of diabetic rats which were intervened later by insulin intensive therapy, and to investigate the mechanism of metabolic memory of hyperglycemia which induced the retina neuropathy in diabetic rats. Methods60 Brown Norway rats were randomly divided into normal control (NC) group, diabetes mellitus (DM) group (6 weeks at DM1, 12 weeks at DM2) and metabolic memory (MM) group, 15 rats in each group. Diabetes was induced by intraperitoneal injection of streptozocin. After 6 weeks, MM group was treated with insulin intensive therapy for 6 weeks. DM1 group was sacrificed at the end of 6 weeks and other groups were sacrificed at the end of 12 weeks. High performance liquid chromatography was used to detect the amount of Glu and GABA in the rat retina. Real-time polymerase chain reaction was applied to quantify the mRNA expressions of Glutamate decarboxylase (GAD). TdT mediated dUTP nick ending labelling was used to detect cell apoptosis. ResultsThe concentration of Glu (t=6.963), GABA (t=4.385) and the ratio of Glu/GABA (t=4.163) in MM group were significantly higher than DM1 group, but the concentration of Glu (t=3.411) and GABA (t=3.709) were significantly lower than DM2 group (P < 0.05). And there was no significant difference in the ratio of Glu/GABA between MM and DM2 groups (t=1.199, P > 0.05). The level of expressions of GAD mRNA in MM group was significantly lower than DM1 group (t=3.496, P < 0.05), but higher than DM2 group (t=8.613, P < 0.05). The number of nerve cells apoptosis in MM group was significantly higher than DM1 group (t=2.584, P < 0.05), but lower than DM2 group (t=3.531, P < 0.05). ConclusionsIntensive therapy later by insulin can partially reduce the content of Glu and GABA and the rate of nerve cells apoptosis, which cannot return to normal levels, and has no effect on the rise in the ratio of Glu/GABA caused by the hyperglycemia. The disorders of Glu and GABA may participate in the metabolic memory of hyperglycemia.