ABSTRACT
AIM: To evaluate the efficacy of selective laser trabeculoplasty (SLT) in glaucomatous eyes with previous incisional glaucoma surgery. METHODS: A retrospective cohort of eyes that underwent SLT at a single institution from 2013-2015 were followed for 1y. Reduction in intraocular pressure (IOP) following SLT was evaluated in eyes with prior trabeculectomy with ExPress mini shunt (Alcon, Ft Worth, TX, USA), Ahmed valve (New World Medical, Cucamonga, CA, USA), or combined phacoemulsification-trabeculectomy. A control group was included with eyes without prior surgery that underwent SLT. Success was defined as >20% drop in IOP from pre-SLT baseline. RESULTS: One-hundred and six eyes were included with 53 in both the prior glaucoma surgery (PGS) and no prior glaucoma surgery (NPGS) groups. Mean pre-SLT IOP was 19.2±4.3 and 20.6±6.0 mm Hg for PGS and NPGS groups, respectively (P=0.17). Both groups produced statistically significant IOP reductions at 1 and 6mo (P<0.04). At 6mo, mean IOP reduction reached 7.3% and 10.8% for the PGS and NPGS groups, respectively (P=0.42). Overall, 27.9% and 31.7% of eyes in PGS and NPGS groups met success criteria at 1y (P=0.70). In the PGS group, eyes with baseline IOP ≥21 mm Hg had IOP reductions of 18.1% (P<0.001), 16.7% (P<0.01), and 8.4% (P=0.31) compared to eyes with baseline IOP <21 mm Hg who had IOP reductions of 2.3% (P=0.39), 3.4% (P=0.19), and 1.1% (P=0.72) at 1, 6mo, and 1y, respectively. CONCLUSION: SLT is efficacious in eyes with prior incisional glaucoma surgery and results in similar IOP reductions compared to eyes without PGS. A larger IOP reduction is observed following SLT in eyes with higher pre-SLT IOP.
ABSTRACT
The experiments test if experimental PE causes red blood cell hemolysis, arginase release and depletion of l-arginine and determine if arginase inhibition preserves l-arginine and improves pulmonary hemodynamics during PE. Experimental PE was induced in male Sprague-Dawley rats by infusing 25 µm microspheres (1.8 million/100 g body wt) in the jugular vein, producing moderate pulmonary hypertension. Pulmonary vascular resistance was estimated from the quotient of the right ventricular peak systolic pressure/cardiac output. Arterial plasma hemoglobin (ELISA), arginase activity (colorimetric assay) and l-arginine (high performance liquid chromatography) were determined. Arginase activity was inhibited by infusion of N-omega-hydroxy-nor-l-arginine (nor-NOHA, 400 mg/kg body wt, i.v.). Values are means ± s.e. Five hours of PE caused red blood cell hemolysis (15-fold increase in plasma hemoglobin) and release of arginase activity (2.7-fold increase). Plasma l-arginine concentration decreased significantly from 250 ± 20.6 to 118 ± 6.0 µmol/L (Control vs. PE) and estimated pulmonary vascular resistance increased 3-fold. Treatment with nor-NOHA prevented the depletion of plasma l-arginine (229 ± 15 µmol/L) and reduced the rise in pulmonary vascular resistance by 40%. In conclusion, experimental PE causes hemolysis, release of arginase activity, depletion of plasma l-arginine and increased estimated pulmonary vascular resistance. Inhibition of arginase activity preserves plasma l-arginine levels and improves estimated resistance, suggesting that the release of arginase during hemolysis contributes to the rise in estimated pulmonary resistance during experimental PE.
