Department of Ophthalmology, Scott and White Eye Institute, Temple, Texas 76504, USA.
Invest Ophthalmol Vis Sci. 2010 Mar;51(3):1583-90. doi: 10.1167/iovs.09-4391. Epub 2009 Oct 22.
Although the arteriolar segment contributes to flow regulation, there is sparse information at the single microvessel level on how vasomotor function is regulated in the human retina. The authors have previously reported vasoreactivity and its underlying mechanisms in isolated porcine retinal arterioles. Herein, they studied human retinal arterioles for comparison.
Retinal tissues were obtained from seven patients undergoing enucleation. Human and porcine retinal arterioles were isolated and pressurized to 55 cm H(2)O luminal pressure for vasoreactivity study using videomicroscopic techniques.
Isolated human and porcine retinal arterioles developed myogenic tone and dilated dose dependently to bradykinin, adenosine, and sodium nitroprusside. Stepwise increases in luminal flow produced graded dilation with approximately 60% dilation at the highest flow tested. Nitric oxide (NO) synthase inhibitor L-NAME nearly abolished dilations to bradykinin and flow and attenuated the adenosine-induced dilation without altering the response to nitroprusside. Endothelin-1 caused dose-dependent constriction. Rho kinase (ROCK) inhibitor H-1152 blocked both myogenic tone and endothelin-1-induced constriction. Responses of retinal arterioles to all agonists and increased flow were similar between pigs and humans.
Isolated human retinal arterioles dilate to bradykinin and increased flow in an NO-dependent manner. NO contributes, in part, to adenosine-induced vasodilation. Conversely, ROCK activation mediates myogenic tone and endothelin-1-induced vasoconstriction. Similarities in these vasoactive responses and the underlying mechanisms between human and porcine retinal arterioles support the latter as a viable experimental model of the human retinal microcirculation.
尽管小动脉段有助于调节血流，但在人体视网膜的单个微血管水平上，关于血管舒缩功能是如何调节的信息很少。作者先前已经报道了在分离的猪视网膜小动脉中血管反应性及其潜在机制。在此，他们研究了人类视网膜小动脉以作比较。
从七名接受眼球摘除术的患者中获得视网膜组织。使用录像显微镜技术，将人类和猪视网膜小动脉分离并加压至 55cmH2O 管腔压力以进行血管反应性研究。
分离的人类和猪视网膜小动脉产生了肌源性张力，并可剂量依赖性地对缓激肽、腺苷和硝普钠扩张。管腔流量的逐步增加产生了分级扩张，在最高测试流量下扩张约 60%。一氧化氮（NO）合酶抑制剂 L-NAME 几乎完全消除了缓激肽和流量引起的扩张，并减弱了腺苷诱导的扩张，而不改变对硝普钠的反应。内皮素-1（ET-1）引起剂量依赖性收缩。Rho 激酶（ROCK）抑制剂 H-1152 阻断了肌源性张力和 ET-1 诱导的收缩。视网膜小动脉对所有激动剂和增加的流量的反应在猪和人之间相似。
分离的人类视网膜小动脉以依赖一氧化氮（NO）的方式对缓激肽和增加的流量扩张。NO 部分促进了腺苷诱导的血管舒张。相反，ROCK 激活介导了肌源性张力和内皮素-1 诱导的血管收缩。人类和猪视网膜小动脉之间这些血管活性反应和潜在机制的相似性支持后者作为人类视网膜微循环的可行实验模型。
