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Changes in Hydrogen Sulfide Concentrations in Porcine Ocular Anterior Segment Explants Under Elevated Perfusion Pressures: Role Of Prostaglandins
Author(s) -
Robinson Jenaye,
Mitchell Leah,
Nguyen Olivia,
Opere Catherine,
Ohia Sunny,
NjieMbye Ya Fatou
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.1271.5
Subject(s) - trabecular meshwork , chemistry , perfusion , cyclooxygenase , explant culture , in vivo , methylene blue , intraocular pressure , flurbiprofen , aqueous humor , ex vivo , endocrinology , medicine , in vitro , pharmacology , enzyme , surgery , ophthalmology , biochemistry , biology , catalysis , microbiology and biotechnology , photocatalysis
We have evidence that H 2 S donors can reduce intraocular pressure in rabbits presumably by increasing aqueous humor (AH) outflow. The aim of the present study was to assess the contribution of H 2 S present in tissues of the trabecular meshwork in the observed increase in AH outflow facility in an ex vivo porcine anterior segment model. Methods Porcine ocular anterior segment explants were perfused with Dulbecco's Modified Eagle's Medium maintained at 37° C and gassed with 5% CO 2 and 95% air, under an elevated pressure of 15 mm Hg for four hours. Perfusates from the anterior segment explants were collected and immediately assayed for their H 2 S content using the well‐established Methylene Blue assay. In some experiments, explants were perfused with cyclooxygenase (COX) inhibitors [flurbiprofen (30 μM) and indomethacin (10 μM)]. The concentration of H 2 S was also measured in the AH (as positive control), and at normal perfusion pressure of 7.35 mmHg in the absence of COX inhibitors. Results Increasing perfusion pressure from 7.35 to 15 mm Hg significantly ( p < 0.001) increased H 2 S concentrations from 0.4 ± 0.1 to 67.6 ± 3.6 nM/μg protein. As a reference value, the H 2 S concentration in the AH was 1.5 ± 0.2 nM/μg protein. In the presence of the COX inhibitors, flurbiprofen (30 μM) and indomethacin (10 μM), the effects of elevated pressure on H 2 S levels were significantly ( p < 0.001 ) reduced from 67.6 ± 3.6 to 0.8 ± 0.1 and 4.2 ± 0.68 nM/μg protein, respectively. Conclusion We conclude that the elevated perfusion pressure‐induced increase in H 2 S concentrations in the perfusate is dependent upon the endogenous production of prostaglandins. However, the exact mechanism whereby elevated perfusion pressures leads to changes in basal H 2 S is unknown and merits further investigation.