Oculohypotensive血管紧张素转换酶抑制剂的效果在急性和慢性青光眼模型。
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梅塔沙GB,沙玛,AA, Goyal家乡
Oculohypotensive血管紧张素转换酶抑制剂的效果在急性和慢性青光眼模型。
J Cardiovasc杂志。2000年8月,36 (2):169 - 75。
- PubMed ID
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10942157 (在PubMed]
- 文摘
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我们学习了各种血管紧张素转换酶(ACE)抑制剂的影响在眼内压(IOP)的兔子实验诱导眼高血压及其作用机理。急性眼高血压是引起注入5%的葡萄糖(15毫升/公斤)通过边际耳脉,而诱发的小鼠慢性青光眼是alpha-chymotrypsin进入眼睛的后室。眼压测量眼压计。血管紧张素转换酶抑制剂都灌输在无菌溶液局部的眼睛。血管紧张素转换酶抑制剂的影响也进行了研究血清胆碱酯酶(真与伪)和ACE酶体外。依那普利、ramiprilat fosinopril产生时间降低眼压的急性和慢性模型眼高血压的兔子。观察眼压的降低> 4 h,并减少的程度相媲美,毛果芸香碱和倍他洛尔。高活性卡托普利和雷米普利IOP未能产生任何变化。洛沙坦也产生了显著降低眼压的慢性模型眼高血压兔子。所有这三个ACE抑制剂抑制ACE活性在房水中被发现。 The enzyme cholinesterase was found to be inhibited by enalaprilat, ramiprilat, and fosinopril. However, atropine did not alter the IOP-lowering effect of enalaprilat in rabbits. Indomethacin pretreatment produced slight but significant inhibition of the IOP-lowering effect of enalaprilat in rabbits. Our data suggest that ACE inhibitors enalaprilat, ramiprilat, and fosinopril produce a significant ocular hypotensive effect in acute and chronic models of ocular hypertension in rabbits. Inhibition of ACE in aqueous humor, and in ocular tissues, resulting in reduced angiotensin II formation, could be one of the major mechanisms responsible for the IOP reduction by ACE inhibitors in rabbits.