Wong Vickie H, Armitage James A, He Zheng, Hui Flora, Vingrys Algis J, Bui Bang V
Department of Optometry and Vision Sciences, University of Melbourne, Melbourne, Australia.
Ophthalmic Physiol Opt. 2015 Mar;35(2):125-34. doi: 10.1111/opo.12174. Epub 2014 Dec 20.
To assess ocular blood flow responses to acute IOP stress following 4 weeks of chronic IOP elevation in streptozotocin (STZ)-induced diabetic and control rats. We hypothesise that chronic IOP elevation for 4 weeks will further impair blood flow regulation in STZ-induced diabetic rats eyes.
Two weeks following citrate buffer or STZ-injections chronic IOP elevation was induced in Long Evans rats via fortnightly intracameral injections of microspheres (15 μm) suspended in 5% polyethylene glycol. IOP was monitored daily. Electroretinography (ERG, -6.79-2.07 log cd s m(-2) ) was undertaken at Week 4 to compare photoreceptor (RmPIII ), ON-bipolar cell (Vmax ) and ganglion cell dominant ERG [scotopic threshold response (STR)] components. 4 weeks post-chronic IOP induction, ocular blood flow (laser Doppler flowmetry) was measured in response to acute IOP challenge (10-100 mmHg, in 5 mmHg steps, each 3 min).
Four weeks of chronic IOP (mean ± S.E.M., citrate: 24.0 ± 0.3 to 30.7 ± 1.3 and STZ-diabetes: 24.2 ± 0.2 to 31.1 ± 1.2 mmHg) was associated with reduced photoreceptor amplitude in both groups (-25.3 ± 2.2% and -17.2 ± 3.0%, respectively). STZ-diabetic eyes showed reduced photoreceptor sensitivity (citrate: 0.5 ± 1.8%, STZ-diabetic: -8.1 ± 2.4%). Paradoxically ON-bipolar cell sensitivity was increased, particularly in citrate control eyes (citrate: 166.8 ± 25.9%, STZ-diabetic: 64.8 ± 18.7%). The ganglion cell dominant STR was not significantly reduced in STZ-diabetic rats. Using acute IOP elevation to probe autoregulation, we show that STZ-diabetes impaired autoregulation compared with citrate control animals. The combination of STZ-diabetes and chronic IOP elevation further impaired autoregulation.
STZ-diabetes and chronic IOP elevation appear to be additive risk factors for impairment of ocular blood flow autoregulation.
评估链脲佐菌素(STZ)诱导的糖尿病大鼠和对照大鼠在慢性眼压升高4周后,眼部血流对急性眼压应激的反应。我们假设,4周的慢性眼压升高会进一步损害STZ诱导的糖尿病大鼠眼部的血流调节。
在柠檬酸盐缓冲液或STZ注射两周后,通过每两周前房注射悬浮于5%聚乙二醇中的微球(15μm),诱导Long Evans大鼠慢性眼压升高。每天监测眼压。在第4周进行视网膜电图(ERG,-6.79 - 2.07 log cd s m(-2))检查,以比较光感受器(RmPIII)、ON双极细胞(Vmax)和神经节细胞主导的ERG [暗视阈值反应(STR)]成分。在慢性眼压诱导4周后,测量眼部血流(激光多普勒血流仪)对急性眼压挑战(10 - 100 mmHg,以5 mmHg步长,每次3分钟)的反应。
4周的慢性眼压(平均值±标准误,柠檬酸盐组:24.0±0.3至30.7±1.3,STZ糖尿病组:24.2±0.2至31.1±1.2 mmHg)与两组光感受器振幅降低相关(分别为-25.3±2.2%和-17.2±3.0%)。STZ糖尿病大鼠的眼睛光感受器敏感性降低(柠檬酸盐组:0.5±1.8%,STZ糖尿病组:-8.1±2.4%)。矛盾的是,ON双极细胞敏感性增加,特别是在柠檬酸盐对照组的眼睛中(柠檬酸盐组:166.8±25.9%,STZ糖尿病组:64.8±18.7%)。STZ糖尿病大鼠中神经节细胞主导的STR没有显著降低。使用急性眼压升高来探测自身调节,我们发现与柠檬酸盐对照动物相比,STZ糖尿病损害了自身调节。STZ糖尿病和慢性眼压升高的组合进一步损害了自身调节。
STZ糖尿病和慢性眼压升高似乎是眼部血流自身调节受损的叠加危险因素。