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

本文研究了前列腺素(PGs)、肾上腺素能药物、过氧化氢及其他与内脏和眼内手术有关的物质对牛眼流出设施、培养的小梁网(TM)形状和牛睫状肌反应的影响。用Crean等人的方法分离培养牛TM组织。用相差显微镜观察细胞，多巴酚丁胺使融合的TM细胞从通常的多边形变为典型的星形。沙丁胺醇无效。抑制剂中的磷酸二酯酶(PDE)是导致这种形状变化的非常有效的途径。肾上腺素、异丙肾上腺素或沙丁胺醇不增加流出功能。设施是97.3([SY.+-]。[)6.8(1微米)，80，8(正弦+-)。[)5.9(10微米)，80，8(正弦+-)。[)5.9(10微米)，83.5(正弦+-)。在β1激动剂多巴酚丁胺的情况下，分别为4.7%(100微米)。相比之下，H202使设备增加了46.5([sy.+-]。[)6.5%(含H202)和22.1()SY+-。[)7.2%(不含H202)，特别是在3-氨基三唑(3AT)和BCNU存在的情况下，PGs也增加了这种便利性，特别是在吲哚美辛存在的情况下。高浓度的β-肾上腺素能药物需要产生即使是微小的流出设施变化，细胞的形状和睫状肌的伴随反应反对肾上腺素能受体的参与。这种机制可以用不同于β作用的不同解释。PDE抑制、PG和/或氧化应激对流出通道及其周围有很大的影响，到目前为止，还没有成功地证明这种影响在体外动物眼的易用性。然而，这项研究表明，这种生物物质可能会减少与侮辱或眼内手术有关的眼部流出能力，可能导致无法治愈的青光眼。

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.