[Endothelial dysfunction in patients with open-angle glaucoma and atheromatous lesions]. / Disfunctia endoteliului vascular la pacienti cu glaucom primar cu unghi deschis si leziuni ateromatoase asociate.

UNLABELLED: A number of observations revealed that the haemodynamic alteration may contribute to pathogenesis of glaucomatous neuropathy. Endothelial dysfunction associated with atherosclerosis impaired the endothelial dependent vasodilatation. PURPOSE: To evaluate the relationship between the endothelial dysfunction (assessed by plasma NO level) and carotid stenosis degree în primary open angle-glaucoma patients. METHODS: Carotid ultrasonography and plasma NOx level (nitrite and nitrate) were obtained from 3 groups of patients: group 1-patients with primary open angle-glaucoma and carotid stenosis; group 2-patients with carotid stenosis and group 3-healthy subjects. RESULTS: A significant lower NO level (compared with group 3) and a significant higher carotid stenosis (compared with group 2) were found în primary open angle-glaucoma patients. There was a significant correlation between the NOx level and carotid stenosis. CONCLUSIONS: Assessing the carotid atherosclerotic plaques may be benefical for the patients with primary open angle-glaucoma. Pharmacological neuroprotection with NO precursors may be useful for the patients with carotid stenosis associated with primary open angle-glaucoma.

[The neurogenic mechanisms of ocular inflammation and their modulation under local treatment with indomethacin]. / Mecanisme neurogene ale inflamatiei oculare si modularea lor sub tratament local cu indometacin.

Neurogenic modulation of the inflammation is an essential mechanism of initiate and conditionate an inflammatory reaction. SP, NKA and NKB--neurokinins are involved in the modulation of the local ocular inflammation initiated by the surgical perforating trauma of the anterior pole. They determine the increase of vascular permeability and the breakdown of the aqueous-humor-blood barrier by direct action on the endothelial vascular receptors and by indirect mechanism (releases prostaglandins). This effect is demonstrated by the increase of the blue Evans concentration in the aqueous-humor after local application of SP, NKA and NKB in a dose-dependent manner. Local treatment with non-steroidal-antiinflammatory drugs like Indomethacin stabilizes the aqueous-humor-blood barrier, by diminishing the local effect of neurokinins. By increasing the vascular permeability SP, NKA and NKB make an important linkage by which the nervous system mediators contribute to the modulation of eye inflammatory responses whose intimate mechanisms are not entirely known yet.