Experimental Study on Aqueous Outflow of the Animal Eyes relating Insults and Intraocular Surgery

研究了前列腺素（pg）、肾上腺素能药物、过氧化氢和其他与损伤和眼内手术有关的物质暴露后，灌注牛眼流出设施、培养小梁网（TM）形状和牛睫状肌反应的变化。采用Crean等人的方法分离培养牛TM组织。用相衬显微镜监测细胞。多巴酚丁胺使融合型TM细胞由通常的多角形变为典型的星状。沙丁胺醇无效。抑制剂中的磷酸二酯酶（PDE）在产生这种形状变化方面非常有效。肾上腺素、异丙肾上腺素或沙丁胺醇不增加流出设施。多巴酚丁胺（一种β - 1激动剂）的剂量分别为97.3(]SY.+- . [)6.8 (1 μ m), 80,8(]SY.+- . [)5.9 (10 μ m), 80,8(]SY.+- . [)5.9 (10 μ m), 83.5(]SY.+- . [)4.7% （100 μ m）。与H202相比，H202能提高46.5(]SY.+-[)6.5%（含H202）和22.1 (]SY.+-[)7.2%（不含H202），特别是在3氨三唑（3AT）和BCNU存在时。pg也增加了设施，特别是在吲哚美辛存在的情况下。高浓度的β -肾上腺素能制剂即使在流出设施、细胞形状和睫状肌的伴随反应中产生很小的变化也需要，这反对肾上腺素能受体介导的参与。这种机制可能与β作用有不同的解释。PDE抑制、PGs和/或氧化应激对流出通道及其周围有很大影响。到目前为止，还没有成功地在体外证明对动物眼睛功能的影响。然而，这项研究表明，这种生物物质可能会减少与损伤或眼内手术有关的眼睛流出设施，可能导致无法治疗的青光眼。

Changes in the outflow facility of perfused bovine eyes, in the shape of cultured trabecular meshwork (TM) and in the responses of the bovine ciliary muscles have been studied after exposure to prostaglandins (PGs), adrenergic drugs, hydrogen peroxides and other substances relating insults and intraocular surgery. Bovine TM tissues were isolated and cultured by the method of Crean et al. Cells were monitored by phase-contrast microscopy.Dobutamine caused confluent TM cells to change from their usual polygonal shape to a characteristic stellate shape. Salbutamol was without effect. The phosphodiesterase (PDE) in hibitors were very effective in producing this shape change. Epinephrine, isoproterenol or salbutamol did not increase the outflow facility. The facility was 97.3(]SY.+-。[)6.8 (1 muM), 80,8(]SY.+-。[)5.9 (10 muM), 80,8(]SY.+-。[)5.9 (10 muM), 83.5(]SY.+-。[)4.7% (100 muM), respectively, in the case of dobutamine, a beta1 agonist. By contrast, H202 increased facility by 46.5(]SY.+-。[)6.5% (with H202) and 22.1 (]SY.+-。[)7.2% (without H202), especially in the presence of 3 amnotriazole (3AT) and BCNU.PGs also increased the facility, especially in the presence of indomethacin.The high concentrations of beta-adrenergic agents required to produce even a small change in outflow facility, the cell shape and the accompanying response of ciliary muscles argue against the involvement of adrenergic receptor mediation. The mechanism may be alternatively explained different from beta action. PDE inhibition, PGs and/or oxidative stress playd great influence on and around the outflow channels.So far, there has been no success in demonstrating such an effect on facility of animal eyes in vitro. However, this study suggests a possibility that such biological substances maay reduce outflow facility of the eye in relation to insults or intraocular surgery, possibly causing untreatable glaucoma.