L Gan1, P Fagerholm. 1. St. Eriks Eye Hospital, Karolinska Institute, Stockholm, Sweden. lisha.gan@ood.ki.se
Abstract
PURPOSE: To study the early events in corneal neovascularization after alkali injury and their relationship to the presence and absence of leukocytes. METHODS: A standardized 5.5-mm diameter penetrating central corneal alkali wound was induced in one eye in each of ten New Zealand white rabbits (2.5 kg). In five of the ten rabbits, 1.5 mL 5% fucoidin was given intravenously every 2 hours to prevent leukocytes from leaving the blood stream. Presence of hyaluronan (HA) and proliferating cell nuclear antigen (PCNA) in the corneas were analyzed using immunohistochemical staining 36 hours after injury. RESULTS: In the alkali wounded corneas, HA was expressed intensively in the limbal area where a massive infiltration of leukocytes was seen. PCNA was expressed in the vascular endothelium as well as in the corneal cells. In the leukocyte-free corneas, HA staining intensity and distribution were the same as in uninjured corneas. No positive PCNA staining was seen in the vascular endothelial cells in these corneas. CONCLUSIONS: Extravasated leukocytes in the alkali-burned corneas caused enhanced production of HA and proliferation of vascular endothelial cells.
PURPOSE: To study the early events in corneal neovascularization after alkali injury and their relationship to the presence and absence of leukocytes. METHODS: A standardized 5.5-mm diameter penetrating central corneal alkali wound was induced in one eye in each of ten New Zealand white rabbits (2.5 kg). In five of the ten rabbits, 1.5 mL 5% fucoidin was given intravenously every 2 hours to prevent leukocytes from leaving the blood stream. Presence of hyaluronan (HA) and proliferating cell nuclear antigen (PCNA) in the corneas were analyzed using immunohistochemical staining 36 hours after injury. RESULTS: In the alkali wounded corneas, HA was expressed intensively in the limbal area where a massive infiltration of leukocytes was seen. PCNA was expressed in the vascular endothelium as well as in the corneal cells. In the leukocyte-free corneas, HA staining intensity and distribution were the same as in uninjured corneas. No positive PCNA staining was seen in the vascular endothelial cells in these corneas. CONCLUSIONS: Extravasated leukocytes in the alkali-burned corneas caused enhanced production of HA and proliferation of vascular endothelial cells.
Authors: Mohammad Nasser Hashemian; Hadi Z Mahrjerdi; Mehdi Mazloumi; Mona S Safizadeh; Yadollah Shakiba; Firouzeh Rahimi; Mohsen Afarideh; Mohamad Ali Zare; Mohammadreza Fallah Tafti; Bahram Bohrani Sepidan; Mohammad Ali Abtahi; Seyed-Hossein Abtahi Journal: J Res Med Sci Date: 2017-02-16 Impact factor: 1.852